Tag Archives: magnetic resonance imaging

Isolated, nondisplaced medial cuneiform fractures: Report of two cases

by Koun Yamauchi MD1*, Satoru Miyake MD1, Chisato Kato MD1, Takayuki Kato MD1

The Foot and Ankle Online Journal 10 (2): 1

Isolated, nondisplaced medial cuneiform fractures are difficult to diagnose using plain radiographs. Computed tomography (CT) or magnetic resonance imaging (MRI) are necessary to aid in diagnosis. This paper describes two patients with this fracture that were more difficult to suspect because the fractures occurred during running, which are extremely rare. Tenderness and swelling around the medial cuneiform was observed that led to suspicion of a fracture; this lead us to perform a CT scan or MRI for confirming the presence of the fracture. However, tenderness and swelling around the midfoot can be observed in a patient with a sprain without the fracture. Therefore, it is more important to note that isolated, nondisplaced medial cuneiform fracture can be induced by an indirect force such as that occurring while running.

Keywords isolated medial cuneiform fractures, non-displaced, during running, computed tomography, magnetic resonance imaging

ISSN 1941-6806
doi: 10.3827/faoj.2017.1002.0001

1 – Department of orthopedic surgery, Akita Hospital, Takara, Chiryu City, Aichi 472-0056, Japan.
*Corresponding author: Koun Yamauchi, koun_yamauchi@yahoo.co.jp

Here, we describe two consecutive patients with isolated, nondisplaced medial cuneiform fractures that occurred during running. Cuneiform fractures generally occurs along with other fractures of the midfoot, such as Lisfranc dislocation fractures, whereas the occurrence of isolated medial cuneiform fracture is rare. A total of only seven published case reports have been reported in the literature [1-5]. Nevertheless, an isolated, non-displaced fracture of the medial cuneiform may be easily suspected when the midfoot has been bruised by a direct, intense force, such as the impact of a traffic accident. However, it may be more difficult to suspect the fracture when being caused by indirect and acute force. Only one case report clearly describes the mechanism of isolated, nondisplaced medial cuneiform fracture being caused by indirect and acute force that occurred during dancing [4]. Therefore, the occurrence of isolated medial cuneiform fracture during running is extremely rare.

Case Report #1

A 25-year-old woman visited a hospital after hearing a cracking sound and feeling pain in her right midfoot during short-distance running at full speed in a park. Clinicians at the hospital diagnosed her injury as a sprain because they found no indications of fracture. Two days later, she visited our hospital with tenderness and swelling around the midfoot. However, radiograph of the midfoot showed no indications of a fracture (Figure 1), and we diagnosed her injury as a sprain.

Figure 1 Plain radiographs of the foot in first case. White arrows show cuneiform bone. (a) anterior–posterior image; (b) lateral–medial image; (c) oblique, lateral–medial image; and (d) oblique, medial–lateral image.

Five days later, she came for an examination; the tenderness and swelling around the midfoot persisted, although the spontaneous pain was gradually decreasing. We performed a computed tomography (CT) scan, which indicated an isolated, nondisplaced medial cuneiform fracture (Figure 2).

Figure 2 Computed tomography of the foot in the first patient. White arrows show fracture line. Dotted lines in axial image (a) show reference lines for coronal image (b) and sagittal image (c).

Her treatment included non weight-bearing (NWB) activity for two weeks without any immobilization. An arch support was applied on her right foot. Partial weight-bearing (PWB) activity was allowed from the fourth week after the injury, full weight-bearing (FWB) activity was allowed from the sixth week after the injury, and she was treated in rehabilitation from the fourth week to three months after the injury. At two months after injury, her hallux range of motion (ROM) recovered to the level of the contralateral side hallux ROM; however, swelling around the midfoot persisted but disappeared at three months after injury. We conducted a self-score, self-administered foot evaluation questionnaire (SAFE-Q) at two and three months after the injury [6]. The following were the scores at two and three months after injury, respectively: Pain scores: 54.1 and 76.4; activities of daily living (ADL) scores: 65.9 and 91.0; social functioning scores: 0.4 and 82.5; shoe-related scores: 41.7 and 91.7; and general health scores: 60 and 90.0 (Full score for each subscale was 100 points).

Case Report #2

A 35-year-old woman presented at our hospital with tenderness and swelling around the midfoot. She had felt sharp pain in her right midfoot as she dashed up an acute slope. Radiographs taken during first examination showed no indication of a fracture (Figure 3), but CT scan showed an isolated, nondisplaced medial cuneiform fracture (Figure 4). Furthermore, magnetic resonance imaging (MRI) showed an acute fracture of the medial cuneiform (Figure 5).

Figure 3 Plain radiographs of the foot in second patient. White arrows show cuneiform bone. (a) anterior–posterior image; (b) lateral–medial image; (c) oblique, lateral–medial image; and (d) oblique, medial–lateral image.

Figure 4 Computed tomography of the foot in the second patient. White arrows show fracture line. Dotted lines in axial image (a) show reference lines for coronal image (b) and sagittal image (c).

Figure 5 Magnetic resonance imaging (MRI) of the foot in the second patient. White arrows show fracture area in coronal images of T1-weighted image (a), T2-weighted image (b), and T2-weighted image with fat saturation sequence (c).

Her treatment included NWB activity for three weeks and immobilization with a soft-splint because of significant swelling. At three weeks after the injury, we started the same treatment strategy as that with the first patient. At two months after injury, her hallux ROM had recovered to the level of contralateral side hallux ROM, and swelling around the midfoot was no longer apparent. SAFE-Q scoring was conducted at 2, 3, and 8 months after injury. Following were the scores at 2, 3, and 8 months after injury, respectively: Pain scores: 76.7, 91.4, and 99.9; ADL scores: 75.0, 93.2, and 97.7; social functioning scores: 83.3, 82.4, and 100; shoe-related scores: 83.3, 58.3, and 91.7; and general health scores: 80, 90.0, and 100.


Similar to earlier reports on diagnosis and treatment of an isolated, non-displaced medial cuneiform fracture [1-5], we were not able to diagnose the fracture in either of our patients based on the plain radiographs alone. All authors have reported that it was difficult to diagnose an isolated, non-displaced medial cuneiform fracture using plain radiographs and that CT and MRI were necessary to diagnose this fracture.

Observed tenderness and swelling around the medial cuneiform bone lead to suspicion of a fracture; this lead us to perform a CT scan or an MRI for confirming the presence of the fracture. An isolated, non-displaced fracture of the medial cuneiform may be easily suspected when the midfoot has been bruised by a direct, intense force, such as the impact of a traffic accident, whereas the stress fracture of this bone can be suspected when the feet of athletes are subjected to repetitive, physical loads. However, when the midfoot is subjected to indirect and acute one-time force, such as dancing or running, clinicians may not perform a CT scan or MRI because they generally do not suspect the occurrence of a fracture, thereby diagnosing the tenderness and swelling around the midfoot as a sprain and/or bruise. Therefore, our suspicion of the isolated, nondisplaced medial cuneiform fracture is noteworthy even when the patient’s midfoot has been subjected to indirect and acute one-time force during running. Although the bipartition of the medial cuneiform was not observed in both our patients, a clinician should suspect the presence of midfoot pain related to the bipartition of the medial cuneiform bone as a differential diagnosis. Steen et al [7] proposed that the bipartition of the medial cuneiform can be associated with midfoot pain following an acute injury.

As reported in the earlier reports, treatment for isolated, nondisplaced medial cuneiform fracture can be conservative [3, 5]. In both of our patients, CT scan taken at five weeks after injury exhibited bony union without complications, such as malunion or displacement. Although the patient’s hallux ROM showed recovery two months after injury, SAFE-Q scores remained unfavorable. In particular, SAFE-Q scores of the first patient were worse, which could have resulted from persistent swelling around her midfoot. At three months after injury, the SAFE-Q scores were better in both patients, except the shoe-related scores of the second patient. We were not able to ascertain any causes for the low shoe-related scores in the second patient. At eight months after injury, the SAFE-Q scores were almost full scores in the second patient, while the SAFE-Q scores were not conducted in the first patient.

Interestingly, CT scan exhibited a similar fracture type in both patients: dorsal and plantar bone fragment with avulsion fracture of the lateral–distal–plantar cortex. Because the fractures in both patients included joint surfaces (navicular–cuneiform joint and cuneiform–metatarsal joint), bone fragment displacement was contraindicated. Therefore, surgery using embedded screws may be an appropriate treatment option for fixation of dorsal and plantar bone fragments. Surgery, such as definitive fixation, is likely to maintain non-displacement until bony union is achieved. Definitive fixation is particularly appropriate for athletes because it enables early and successful recovery (because athletes are able to actively return to their respective sports sooner) compared to conservative treatment. We strongly suggest that more study is needed to assess the effect of surgical treatment options on recovery after isolated, nondisplaced medial cuneiform fracture.


Isolated medial cuneiform fracture can be induced by an indirect force while running and should be diagnosed by CT and MRI.


Ethical approval: All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed consent:  Informed consent was obtained from all individual participants included in the study.

Funding declaration and Conflict of Interest:  This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. There are no conflicts of interest to declare.


  1. Olson RC, Mendicino SS, Rockett MS. Isolated medial cuneiform fracture: review of the literature and report of two cases. Foot Ankle Int 2000;21(2):150-153. (PubMed)
  2. Taylor SF, Heidenreich D. Isolated medial cuneiform fracture: a special forces soldier with a rare injury. South Med J 2008;101(8):848-849. (PubMed)
  3. Guler F, Baz AB, Turan A, Kose O, Akalin S. Isolated medial cuneiform fractures: report of two cases and review of the literature. Foot Ankle Spec 2011;306–309. (PubMed)
  4. Liszka H, Gadek A. Isolated bilateral medial cuneiform fracture: a case report. Przegl Lek 2012;69(9):708-710. (PubMed)
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Schwannoma: A case report

by Mark J. Mendeszoon, DPM, FACFAS, FACFAOM1 , Natalie Cunningham, DPM2 , Robert S Crockett, DPM3 , Donald Kushner, DPM4

The Foot and Ankle Online Journal 2 (10): 4

Schwannomas are tumors derived from the myelin sheath of nerves. As schwannomas grow they can displace and compress nerves causing pain, weakness and numbness. Schwannomas usually exist as a solitary mass and can occur at random. Having no racial or sexual predilection, schwannomas usually occur in individuals between the ages of 20-50 years old. The most common sites for schwannomas are the head, flexor surfaces, upper extremity, lower extremity and trunk. It is very rare for schwannomas to become malignant, but surgery is still the principal treatment to eliminate symptoms that may persist and to correctly diagnosis the tumor. We discuss one case of a schwannoma found in the foot.

Key Words: Schwannoma, neurilemmona, peripheral nervous system tumors, Magnetic resonance imaging.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot and Ankle Online Journal (www.faoj.org)

Accepted: September, 2009
Published: October, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0210.0004

Verocay was one of the first to describe a nerve tumor derived from the myelin sheath in 1908, termed neurinoma. [5] Later in 1935, Stout reported on tumors arising from the nerve sheath and specifically described tumors of neuroectodermal origin. [1 ]The neuroectoderm consist of Schwann cells and collagen fibers. [2] Schwannomas are tumors that arise from the myelin sheath of nerves and are the most common solitary nerve tumor of the body. [3]

Schwannomas can be found in various parts of the body with the most common site being the head. However, in the lower extremity they are most commonly found in the deep tissues of the foot. [10] Unlike neurofibromas, Schwannomas rarely metastasize. [4] As a schwannomas grows along the nerve sheath the fibers begin to push outward.

Studies relate a correlation between size of the nerve trunk and size of the lesion.[7] Lesions can be small or large, usually with a diameter less than 8cm when located in the foot. [11,12] Clinical evaluation of symptoms is sometimes a great indicator of what the lesion may be, but Magnetic Resonance Imaging (MRI) of the lesion is standard for obtaining differential diagnosis and determining the size and depth of the lesion. Once a lesion of this type is identified on MRI it must be surgically removed. The specimen is then sent to pathology, which allows the definitive diagnosis of Schwannoma.

Case Report

A 56 year-old female with a past medical history of hypertension, depression, and hypothyroidism first presented at age 54 with complaints of left foot pain and swelling of about one year duration. She related that she was bitten by a bug in the Caribbean and had swelling and discomfort since then. She denied any injury or trauma.

She also denied constitutional signs of infection. Initial radiographs failed to reveal any bony abnormalities or tumor like masses. The patient was then treated conservatively with an NSAID and change of shoe gear. A year later she returned complaining of an increase in the size of the left foot. She explained that her symptoms had never completely resolved and she noticed that her left foot was getting larger and more painful in her shoes which also were not fitting properly. An MRI was obtained which identified a large cystic lesion beneath the metatarsals extending from the cuboid to the metatarsophalangeal joints. (Figs.1 A – F) The lesion measured 8.0cm length, 2.8cm in depth and 3.1cm in width. The lesion coursed distally between the first and second metatarsals. Following the MRI the patient was scheduled for surgical removal of the mass in her left foot. (Figs.2 and 3) Initial histological report suggested neurofibromatosis but further analysis determined the lesion was a schwannoma with no evidence of sarcomatous transformation. The patient’s swelling was resolved within several weeks but she continued to complain of numbness between the first and second metatarsals. This was an ongoing complaint up to 5 months post-operatively. At that time she was told that she may have some permanent numbness, which is not uncommon for a lesion of this size and in this area.

Figure 1A.- F.  Sagittal, Axial and coronal T1, T2, gradient echo/inversion recovery sequences were performed on MRI. (A-F)  A very large cystic fluid collection plantarly, deep to the metatarsal bones,  extending from the cuboid posteriorly, to the proximal metatarsophalangeal junction. (A-F)  Lesion invaginates between 1st and 2nd metatarsals with some upward extension. Adjacent musculature uninvolved, but displaced.  No definitive bony involvement seen. (E and F)


Figures 2A and B. Intraoperative view of Schwannomma being excised from foot. Dorsal view of schwannoma. Attempt to remove the lesion from dorsal approach. (A) Plantar view of schwannoma being removed from between 1st and 2nd metatarsals. (B)

Figure 3 Intraoperative measurement of schwannomaremoved from the plantar left foot. The Schwannoma measures 8cm (with adjacent stump total length 12cm).


Schwannomas are derived from Schwann cells of the neuroectoderm. Their function is to form the myelin sheath of nerves in the peripheral nervous system, which insulates the nerve and facilitates the transmission of an impulse. Also categorized with a neurinoma, neurileomma, or neurofibroma, the schwannoma is a benign encapsulated slow growing tumor. [12,13] Unlike neurofibromas, schwannomas do not traverse through the nerve but remain in the sheath lying on top of the nerve. They have a low risk of metastasizing and do not usually present with underlying systemic disease, such as neurofibromatosis. Schwannomas were found to have some transmission types that were autosomal dominant. [13] As mentioned previously, schwannomas are most common in patients in the second through the fifth decades of life and have no gender or racial predilection. [12] Their size ranges from about 2-20cm in diameter with the smaller tumors appearing white, fusiform, round and firm. The larger tumors are usually irregular, lobulated and grey or yellowish white. [9]

Schwannomas can present with no symptoms, mild symptoms or severe symptoms mostly affecting the nerves. The first case of a solitary neurilemma was discussed by Liebau, who stated that schwannomas should be looked for in all cases where patients present with pain, paresthesia of leg and foot, especially if all other injury has been excluded. [14] Much like the case presented above, research agrees that most patients present after a long delay with complaints of an isolated superficial palpable mass. [15] The tumor was encompassing the plantar aspect of the patient’s foot in this case and her main symptoms were swollen foot which induced pain when wearing shoe gear. Schwannomas can also appear throughout the body usually extracranial, but also found in the pelvis, upper and lower extremity. Schwannomas are commonly found on the flexor surface most likely because nerves trunks are generally larger at this aspect. [1,16] Persing, et al., discussed how a proximal invasion of this tumor at the sciatic nerve caused tarsal tunnel like symptoms. [18]

He spoke of how his patient had an unsuccessful tarsal tunnel release then later removal of the schwannoma from the sciatic nerve alleviated all symptoms in the foot. [17] A similar study by Gominak presents a case in which the posterior tibial nerve was thought to be compressed by the flexor retinaculum. [16] Release of the retinaculum was performed ineffectively. It was later determined that the patient had a thigh schwannoma which, when resected, alleviated all lower extremity symptoms. Therefore when a patient presents with pain in the foot and ankle a more proximal tumor should be investigated if symptoms persist after failed treatment. Nerve sheath tumors are usually initially recognized by MRI. They have an intermediate to moderately bright signal on T1-weighted images, and a bright, heterogeneous signal on T2-weighted images. [12] MRI is useful in identifying the exact location and size of the tumor. However, it is impossible to actually diagnose a schwannoma utilizing MRI alone. The tumor must be surgically excised and sent for pathological evaluation. The pathology report will give the definitive diagnosis of schwannoma and establish whether the lesion is benign or malignant. After surgery symptoms should subside but the patient may continue to have paraesthesia, as the above patient. Motor and sensory abnormalities usually return to normal if the schwannoma is found and resected promptly following initial finding. When they are resected the function of the nerve should not be compromised. [13] With most surgical procedures patients are warned of risk of nerve damage, we must especially warn them of an increase in this risk with surgical excision of a schwannoma. The patient in this case study endured several months of post operative numbness. She has been followed since then and relates no symptoms at this time.

In conclusion, schwannomas are rare solitary nerve sheath tumors. They should always be considered as a differential diagnosis when tarsal tunnel syndrome, neuromas, nerve entrapment or radiculopathy18 is suspected. Schwannomas found in the proximal aspect of the lower extremity can also cause distal symptoms or injury, so this must also be considered, especially if the previous differentials have been ruled out. Early diagnosis can prevent permanent nerve damage, soft tissue or boney deformity.


1. Stout AP: The peripheral manifestations of the specific nerve sheath tumor (Neurilemoma) Am J Cancer 24: 751 – 796, 1935.
2. Berlin SJ: Soft Somatic Tumors of the Foot: Diagnosis and Surgical Management. Futura Publishing Co, Mount Kisco, NY: 227, 1976.
3. Stout AP: Tumors of the peripheral nervous system. In Atlas of tumor pathology. Section 2, Fasicle 6. Washington, D.C., Armed Forces Institute of Pathology, 1949.
4. Giannestras NJ, Bronson JL: Malignant schwannoma of the medial plantar branch of the posterior tibial nerve (unassociated with von Recklinghausen’s disease) A Case Report. J Bone Joint Surg 57A (5): 701 – 703, 1975.
5. Verocay J: Zur Kenntnis der Neurofibroma Beitr Pathol Anat 48:1 – 69, 1910.
6. Das Gupta TK, Brasfield RD, Strong EW, Hajdu SI: Benign solitary schwannomas (neurilemomas). Cancer 24: 355 – 366, 1969.
7. Ogose A, Hotta T, Morita T, Yamamura S, Hosaka N, Kobayashi H, Hirata Y: Tumors of peripheral nerves: correlation of symptoms, clinical signs, imaging features, and histologic diagnosis. Skeletal Radiol 28(4):183-8, 1999.
8. Spiegl PV, Cullivan WT, Reiman HM, Johnson KA: Neurilemoma of the lower extremity. Foot Ankle 6 (4): 194 – 198, 1986.
9. Wolpa, ME, Johnson JD: Schwannoma of the fifth digit. J Foot Surg 28 (5): 421 – 424, 1989.
10. Takada E, Ozaki T, Kunisada T, Harada Y, Inoue H: Giant schwannoma of the back. Arch Orthop Trauma Surg 120: 467 –469, 2000.
11. Maleux G, Brys P, Samson I, Sciot R, Baert AL: Giant schwannoma of the lower leg, (Eur) Radiol. 7: 1031 – 1034, 1997.
12. Joyce M, Laing AJ, Mullet H, Mofidi A, Tansey D, Connolly CE, McCabe, JP: Multiple schwannomas of the posterior tibial. Nerve Foot Ankle Surgery 8:101 – 103, 2002.
13. Liebau C, Baltzer AW, Schneppenheim M, Braunstein S,•Koch H, Merk H: Isolated peripheral neurilemoma attached to the tendon of the flexor digitorum longus muscle. Arch Orthop Trauma Surg 123: 98 – 101, 2003.
14. White NB: Neurilemomas of the extremities J Bone Joint Surg 49A: 1605 – 1610, 1967.
15. Masson WP: Experimental and spontaneous schwannomas (peripheral gliomas.) Am J Pathol 8: 367, 1943.
16. Gominak S , Ochoa J: Sciatic schwannoma of the thigh causing foot pain mimicking plantar neuropathy. Muscle and Nerve 21 (4): 528 – 530, 1998.
17. Carpintero P, Gascón E, Abad JA, Ruza M: Foot schwannomas that mimic nerve – Entrapment syndromes a report of three cases. J Am Podiatr Med Assoc 96(4): 344 – 347, 2006.
18. Persing J, Nachbar J, Vollmer D: Tarsal Tunnel Syndrome Caused by Sciatic Nerve Schwannoma. Ann Plast Surg 20 (3) 252 – 255, 1988.

Address correspondence to: Mark Mendeszoon, DPM, Dept. of Surgery, Podiatry Division, Chardon Medical Center, University Hospitals, 13207 Ravenna Rd., Chardon, Ohio 44024

Dept. of Podiatric Surgery, Chardon Medical Center, University Hospital at Geauga, OH.
Submitted while 3rd year resident Dept. of Surgery, Louis Stokes Cleveland VA Medical Center, Cleveland, OH.
Submitted while 3rd year resident Dept. of Surgery, Louis Stokes Cleveland VA Medical Center, Cleveland, OH.
Department of Surgery, Podiatry Division, Louis Stokes Cleveland VA Medical Center, Cleveland, OH.

© The Foot and Ankle Online Journal, 2009

Transient Regional Migratory Osteoporosis in the Ankle and Foot: A case series and literature review

by Simon B.M. MacLean, MRCSEd1 , Raj Kumar, FRCS (Tr&Orth)2 , Timothy M. Clough, FRCS (Tr&Orth)3 , Jeremy P.R. Jenkins, FRCR4 , Jim L. Barrie, FRCS (Tr&Orth)5 , Peter L.R. Wood, FRCS (Tr&Orth)6

The Foot and Ankle Online Journal 2 (10): 1

Transient regional migratory osteoporosis (TRMO) is a rare self-limited syndrome characterized by sudden onset of joint pain, followed by focal osteopenia after a few weeks, with spontaneous recovery. We report six cases of TRMO seen in foot and ankle clinic together with a review of the literature.

Key words: Transient regional migratory osteoporosis, magnetic resonance imaging, reflex sympathetic dystrophy.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot and Ankle Online Journal (www.faoj.org)

Accepted: September, 2009
Published: October, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0210.0001

Transient Regional Migratory Osteoporosis (TRMO) is a migrating arthralgia of the lower limb joints associated with severe intercurrent focal osteoporosis at the involved site. It usually affects healthy middle-aged males, with sudden onset of pain, significant functional impairment, but little in the way of clinical findings. First described in the British literature 50 years ago with indistinct diagnostic features, the availability of advanced imaging now makes the diagnosis more accessible. Cases have previously been described but we report a series of cases in the foot and ankle to promote reader’s awareness of the entity, and to encourage correspondence and discussion on the possible etiology and appropriate management.

Case 1

A 45 year-old male presented with right foot and ankle pain in January 2003. He had no recollection of injury to the foot. Clinically, the ankle was warm, swollen and painful to move. Laboratory studies revealed a normal white cell count and CRP level; the erythrocyte sedimentation rate was moderately elevated at 39. Plain radiographs revealed patchy osteoporosis about the ankle. The initial impression was that this was possibly due to a stress fracture and a Magnetic Resonance Imaging (MRI) scan was ordered on the basis of which a diagnosis of reflex sympathetic dystrophy (RSD) was made and he was referred to a pain clinic. He failed to respond to two guanethidine blocks. Several months later, he developed severe pain in his left hip.

Clinically, movements at the left hip were painfully restricted. Plain radiographs of the left hip showed evidence of patchy osteoporosis. MR scans of the hips showed an oedema-like pattern in the bone of the left upper femur. A bone scan showed marked increased uptake of isotope at the right ankle and throughout the right tarsal region but excluding the right calcaneum.

There was also marked increased uptake of isotope within the left femoral head and less marked increased uptake throughout the left femoral neck and trochanteric region. A biopsy of the right ankle to exclude sinister pathology showed evidence of mild chronic synovitis with no evidence of granuloma formation. At this stage a diagnosis of tuberculosis was considered despite the negative culture and the absence of granuloma formation on biopsy. He was commenced on anti-TB treatment as he had a Heaf test which was strongly positive. A few months later he started to get discomfort in the right knee. At this stage, the right foot and the left hip had improved considerably. Clinically, the right knee was warm and swollen with restricted range of motion. He was mobilizing with crutches at this stage. MR imaging of the right knee performed in September 2003 showed a prominent oedema like pattern in the distal femur, particularly affecting the lateral femoral condyle. There was a small joint effusion, but the appearances did not suggest synovial hypertrophy or soft tissue swelling. Review of all the plain radiographs, the bone and MR scans finally led to the diagnosis of TRMO. In December 2003 he complained of discomfort in the left knee. MR images of the left knee were however normal. Repeat MR images of the ankle showed that it had virtually returned to normal and that there was no lasting damage to the ankle joint.

Case 2

A 53 year-old white female was referred with left ankle and hind foot pain from October 2002. The symptoms were of insidious onset. Plain radiographs of the ankle and hind foot at that stage were unremarkable. (Fig 1) Her symptoms continued to deteriorate over the next 6 months. Physical examination revealed some discoloration of the foot and ankle. There was a small joint effusion about the ankle. Weight bearing was uncomfortable and ankle movements were painful. Laboratory findings were unremarkable. Plain radiographs of the foot and ankle revealed gross osteopenia. (Fig 2) Bone scintigraphy confirmed marked increase in uptake about the foot and ankle (Fig 3). MR imaging of the ankle revealed minor effusion in the ankle and subtalar joints. T1- weighted images revealed low subarticular signals and low signal in the talus and anterior part of the os calcis. The patchy bone marrow signals were reported to be consistent with a diagnosis of RSD or TRMO. Over the next six months the ankle pain settled with physiotherapy, partial weight-bearing and oral analgesia. Eighteen months after the initial presentation, she started developing moderate pain in the ipsilateral knee. Physical examination revealed minor effusion. Plain radiographs and laboratory findings were unremarkable. MR imaging of the knee revealed joint effusion and a diffuse bone marrow oedema pattern consistent with TRMO.

Figure 1 Anterior posterior and lateral views of left ankle demonstrating normal bone density.

Figure 2 Comparative radiographs performed 6 months later showing marked osteopenia.

Figure 3 Radioisotope bone scan showing increased uptake in the talar dome and head, and midfoot.

Case 3

A 60 year-old male was referred to our unit with a diagnosis of septic arthritis of the left ankle. He gave a 7-month history of pain and swelling of the ankle. The symptoms were of insidious onset. Physical examination revealed a diffuse swelling about the ankle particularly and increased local warmth. Plain radiographs and laboratory investigations were within normal limits. MR imaging revealed marrow oedema in the talar head, the talar dome and within the anterior aspect of the tibial plafond. (Fig 4) There was soft tissue swelling with effusions in the ankle, subtalar and talonavicular joints. The symptoms resolved considerably over the next six months, although he had residual ankle discomfort.

Figure 4  A curvilinear area of increased signal (arrowed) parallels the articular surface of the talar dome on a coronal T2-weighted STIR image. Note the oedema in the talar body with increased fluid in the sinus tarsi with surrounding soft-tissue oedema.

Case 4

A 34 year-old male was referred with a six-month non-specific hind/midfoot pain following a twisting injury. He was found to be hyperalgesic, with no other signs of chronic regional pain syndrome (CRPS). Physical examination revealed diffuse swelling about the foot and ankle with some tenderness. Laboratory findings were unremarkable. Bone scintigraphy demonstrated increased uptake in the hind/midfoot as well as the left hip. Plain radiographs of the hip revealed an almost healed transcervical femoral neck fracture. MR imaging again showed extensive high signal changes in the hind foot. By this stage he had developed a stress fracture of the 4th metatarsal. The symptoms resolved slowly over 12 months with symptomatic treatment. He is now back at work.

Case 5

A 60 year-old white male was referred for a second opinion. He had been diagnosed with osteomyelitis of the talus. He gave a 9 month history of right hind foot pain. The symptoms were of insidious onset. Plain radiographs revealed generalized osteopenia, with an apparent lytic lesion in the talar neck. Laboratory findings were normal. Bone scintigraphy revealed increased uptake in the hind/midfoot. Labeled white cell scan was negative. MR imaging demonstrated extensive high signal changes and a diagnosis of regional migratory osteoporosis was made by the radiologist. The symptoms resolved slowly. He returned a year later with similar symptoms on the left foot. MR imaging at that stage showed complete resolution on the right. The symptoms eventually settled on both sides at six month follow-up with supportive treatment.

Case 6

A 41 year-old white female was referred for a second opinion on a diagnosis of avascular necrosis of the talus. She gave a 6 month history of generalized hind foot pain following a minor twisting injury. Physical examination and laboratory findings were unremarkable. Plain radiographs revealed osteopenia affecting the calcaneus and the talus. Bone scintigraphy revealed increased uptake in the talus, os calcis and the cuboid. MR imaging demonstrated extensive high signal changes suggestive of TRMO. She was treated symptomatically. At follow-up 12 months from our initial review she continues to have pain and increased sensitivity. (Table 1)

Table 1 Comparison of the cases.


Transient Osteoporosis (TO) is a rare self-limited syndrome characterized by sudden onset of joint pain, followed by focal osteopenia after few weeks, with spontaneous recovery. This was first described by Revault, et al., as a distinct clinical syndrome in French literature and was thought to be due to neurotropic changes, possibly secondary to minor trauma. [1] The first report of this disorder in the English literature was by Curtis and Kincaid in 1959. [2] They described three women who developed hip pain and osteopenia in the last trimester of pregnancy. The symptoms and radiographic changes disappeared spontaneously after several months. Although this was the original description of the phenomenon, none of our cases included pregnant women. By 1968, Lequesne coined the term – transient osteoporosis of the hip. [3] Subsequent reports described similar clinical and radiographic patterns in other locations such as the knee and ankle. [4,5]

TO may present one episode affecting only one joint or recurrent episodes that may affect multiple joints. Multiple joints may be involved in as much as 40% of patients and when this occurs the condition is referred to as transient regional migratory osteoporosis or TRMO. [6]

The aetiology of TRMO remains unclear. Curtis and Kincaid [2] proposed a neurogenic compression hypothesis suggesting that TOH in pregnant women may be determined by a mechanical compression of the obturator nerve. Rosen [7], Arnstein8, Bray, et al., [9] suggested an impairment of venous return and local hyperaemia. Lequesne [3] advocated that TO is caused by non-traumatic form of RSD, a theory supported by Doury. [10] However, TO lacks the vascular and cutaneous changes characteristic of RSD. McCord, et al., [11] reported electromyography (EMG) abnormalities in TRMO, which they associated with the commonly seen muscular atrophies. McCord documented denervation patterns coincident in location and time with TRMO attacks. However other reports [12,13] have suggested normal EMG and nerve conduction studies. One of the likely explanations for the pathogenesis of TO is perhaps that proposed by Frost [14] and others. [15,16] He stated that under noxious tissue stimuli, the ordinary biological processes, including blood flow, cell metabolism and turnover and also tissue modelling and remodelling, might be greatly accelerated, called the Regional Acceleratory Phenomenon (RAP). In his opinion a prolonged or exaggerated RAP in which a large number of bone turnover foci are activated, is the cause of TO. It has been hypothesized that symptoms may be related to bone marrow edema demonstrated at MRI and to a transitory regional arterial hyperflow observed at the early scintigraphic analysis. [17] Bone tissue micro damage is the most frequent noxious stimulus that provokes RAP and bone tissue micro fracture is the main consequence. Several elements support this hypothesis. The repeatedly observed histological findings in patients with TO showing mild inflammatory changes and osteoporosis, associated with an elevated bone turnover with increased bone resorption and reactive bone formation [18,19,20] are a good description of ongoing TRMO.

The timing of the episodes of TO, with an abrupt onset, an acute phase of one or two months, a steady – state period and a final partial and delayed recovery resembles the course of RAP. [21] The intense focal osteoporosis and the following partial bone resorption which occurs even in the absence of loading is in accordance with the temporarily increased remodeling space described in the case of RAP. [14,21]

In TRMO, diagnosis is challenging. In virtually all cases the pain gradually improves and the clinical and radiographic findings resolve in 6- 12 months. [22] Although instances lasting eighteen to twenty-four months have been noted, our cases illustrate two examples of TRMO lasting for 24 months and more. This has not been widely reported previously in the literature. Repeat attacks at adjacent sites are characteristic. Several regions may be affected sequentially or the episodes may overlap. [23,24] Usually all the attacks occur within 1-3 years but episodes occurring 11 – 13 years apart have been reported. [8] Occasionally the phenomenon of RMO can recur within the same joint. There are few reports of RMO affecting different regions of the same joint and in the knee there are reports of TRMO migrating from the lateral femoral condyle to the medial and vice versa. [4,25] The condition is distinguished by its episodic migratory nature. No permanent joint damage results from these acute recurrent episodes.

A painful joint with localized demineralization is suspicious of an inflammatory or neoplastic disease process. The differential diagnosis must include inflammatory arthritis as rheumatoid arthritis, infectious arthritis, osteoarthritis and crystal arthropathy. [8,16,26] Other diagnosis to be considered includes primary bone tumors, osteomyelitis, tuberculous arthritis, multiple myeloma and metabolic bone disease. Synovial chondromatosis of the hip may mimic TO, but the course is long and irreversible. The history, normal laboratory findings and characteristic imaging usually differentiates TRMO. It is often difficult to differentiate from RSD in the early stages. In RSD, there is often a history of trauma or surgery.

Cardinal symptoms are diffuse burning pain in the affected region, sensory disturbances of hypo or hyperaesthesia, trophic changes of discoloration, swelling and thickening, alteration in the skin temperature, autonomic regulation and motor disturbance. [27,28] In the early stages avascular necrosis (AVN) should be ruled out. A long self-limited course, recurrence in other joints and the imaging characteristics help to differentiate AVN from TO. In the early stages the two conditions can be difficult to differentiate, but typically in AVN the pain is present at rest, the limp and antalgic gait are late findings and the functional disability is proportional to the pain level. [29] A prolonged and reversible clinical course, normal laboratory findings, negative cultures and characteristic radiographic findings should lead one to consider RMO after excluding the more common rheumatic diseases and especially infectious arthritis. Vigilance is however required since two authors report cases resembling RMO prior to recognizing tuberculous infection. [3,16] Case 1 illustrates an example where a diagnosis of TB was made before bone biopsies returned as negative for the infection. Tannenbaum, et al., [20] described that in two of their four cases the initial diagnosis was that of septic arthritis even though the patients were afebrile and constitutionally well. Three of our cases had an initial diagnosis with an infective cause for their symptoms (osteomyelitis, TB, septic arthritis) despite the patients being systemically well on presentation. Apart from slightly elevated ESR counts, the laboratory tests came back as normal in each case.

Diagnostic imaging can be challenging also. Little information is available on the quantitative assessment of systemic or local osteoporosis. Recently a precise assessment of the bone mass by quantitative methods has been reported at the lumbar spine in a case of TRMO30 and also at both hips and the lumbar spine in a case of transient osteoporosis of the hip in pregnancy (TOH). [20] In both cases the appraisal of bone loss in sites other than the symptomatic site aroused suspicion of a wider systemic involvement, which has been suggested in recent literature. [23,24,31]

Due to the rarity of the disease and the unpredictability of the episodes, there is only a limited amount of quantitative data about the degree and extent of bone loss. Trevisan, et al., [32] using bone densitometry assessment noted that in four of five acute episodes the decrease in bone mass was greater than 30%. In one episode the decrease in bone mineral content at the involved site was > 75%. With such an extreme decrease in bone mass it is not surprising that fractures have been reported as a complication of acute phase of bone loss in TRMO. [33,34] Case 4 illustrates an example of fracture of the hip (transcervical) occurring as a complication of TRMO. During the acute episode, the bone loss may not be confined to the affected joint but involved the whole lower limb to a greater degree at sites with a predominantly trabecular pattern. The clinical subsidence of the acute phase was accompanied by an increase in the bone mineral density. Case 6 illustrates a patient initially diagnosed with AVN of the talus, then later diagnosed with TRMO on the basis of MRI findings. X-ray appearance of AVN rarely shows diffuse osteopenia and the classical appearance of AVN is a mottled radiolucent area surrounded by an area of sclerosis. Plain radiographs are not useful in the early stages as changes in TO may appear only four to eight weeks after the onset. The increased uptake is usually less intense in AVN and more limited to the femoral head. MR imaging is a useful tool to differentiate between the two conditions. In AVN a focal non-homogenous, segmental and well-demarcated lesion in the anterosuperior subchondral region of the femoral head is the classical appearance. T2- weighted images may demonstrate the double line sign pathognomonic of AVN

Treatment modalities are difficult to assess because the condition is self-limiting. Several reports note favourable results with NSAIDs and glucocorticoids. [15] However several authors found that with glucocorticoids there was no relief of joint pain or alteration of the disease course. [11,35] Clinical and radiographic improvement has been noted with calcitonin [36,37,38], although not universally. [19,23,39]

Antituberculous drugs have failed40 , as have attempts at sympathetic blockade.37,40 Several authors have recommended a conservative, symptomatic approach with protection against full weight bearing. Traumatic fractures of the femoral neck and stress fractures have been infrequently reported in patients with TO.41,42 Some authors have advocated the use of intravenous pamidronate treatment as potential therapy for the condition.35,43 We advocate the approach of mild analgesia with protected weight bearing and physiotherapy designed to enhance muscle function and prevent immobilization. In all our cases symptoms improved only with supportive measures.


Case descriptions of TRMO are not always consistent as TRMO is a rare phenomenon and a diagnosis usually made only after other inflammatory and neoplastic causes have been excluded. We highlight the potential problems in establishing the diagnosis due to its unclear etiology and clinical presentation. By presenting a large series of this condition affecting the foot and ankle, we propose that early bone scan and MR imaging should be considered in patients presenting with vague arthralgic symptoms in the presence of a lack of other constitutional symptoms.


1. Ravault PP, Gainet P, Perthier L, Emery J, Carrier F: Rhumatis mes chroniques de la main et rhumatisme neurotrophique du member superieur. J Med Lyon 28: 363, 1947.
2. Curtis PH, Kincaid WE: Transient demineralisation of the hip in pregnancy. A report of three cases. J Bone Joint Surg 41A: 1327 – 1333, 1959.
3. Lequesne M: Osteoporosis of the hip. A non-traumatic variety of Sudecks atrophy. Ann Rheum Dis 27: 463 – 471, 1968.
4. Parker RK, Ross GJ, Urso JA: Transient osteoporosis of the knee. Skel Radiol 26: 306 – 309, 1997.
5. Swezey RL: Transient osteoporosis of the hip, knee and ankle. Arthritis Rheum 13: 858 – 868, 1970.
6. Crespo E, Sala D, Crespo R, Silvester A: Transient osteoporosis. Acta Orthop Belgica 67(4): 330 – 337, 2001.
7. Rosen R: Transitory demineralisation of the femoral head. Radiology 94:509 – 512, 1970.
8. Arnstein RA: Regional Osteoporosis. Orthop Clin North Am. 3: 585 – 600, 1972.
9. Bray St, Partain CL, Teates CD, Guildford WB, Williamson BRJ, McLaughlin RC: The value of bone scan in idiopathic regional migratory osteoporosis. J Nucl Med 20:1268 – 1271, 1979.
10. Doury P: Bone-marrow oedema, transient osteoporosis and algodystrophy. J Bone Joint Surg 76B: 993 – 994, 1994.
11. McCord WC, Nies KM, Campion DS, Louis JS: Regional migratory osteoporosis: A denervation disease. Arthritis Rheum 21: 834 – 838, 1978.
12. Kaplan SS, Stegman CJ. Transient osteoporosis of the hip. A case report and review of the literature. J Bone Joint Surg 67A: 490 – 493, 1985.
13. Keys Gw, Walters J: Idiopathic transient osteoporosis of the hip: brief report. J Bone Joint Surg 69B 773 – 774, 1987.
14. Frost HM: Perspectives: bone’s mechanical usage windows. Bone Miner 19: 257 – 271, 1992.
15. Duncan H, Frame B, Frost H, Arnstein AR: Regional migratory osteoporosis. South Med J 62: 41 – 44, 1969.
16. Langloh ND, Hunder GG, Riggs BL, Kelly PJ: Transient painful osteoporosis of the lower extremities. J Bone Joint Surg 55A: 1188 – 1196, 1973.
17. Negri G, Grassi S, Zappia M, et al. A new hypothesis for the bone marrow edema pathogenesis during transient osteoporosis. J Orthopaedics and Traumatology 7(4): 176 – 181, 2006.
18. Scapira D: Transient osteoporosis of the hip. Sem Arthr Rheumat 22: 98 – 105, 1992.
19. Lequesne M, Kerboull M, Bensarson M, Perez C, Dreiser R, Forest A: Partial transient osteoporosis. Skeletal Radiol 2: 1 – 9, 1977.
20. Funk JL, Shoback DM, Genant HK: Transient osteoporosis of the hip in pregnancy: natural history of changes in bone mineral density. Clin Endocrinol 43: 373 – 382, 1995.
21. Frost HM: The biology of fracture healing. An overview for clinicians. Part 1. Clin Orthop 248: 283 – 293, 1989.
22. Schils J, Piraino D, Bradford JR, Stulberg B, Belhobek GH, Licata AA: Transient osteoporosis of the hip: clinical and imaging features. Cleve Clin J Med
23. Lakhanpal S, Ginsburg WW, Luthra HS, Hunder GG: Transient regional osteoporosis: a study of 56 cases and review of the literature. Annals Intern Med 106: 444 – 450, 1987.
24. Mavichak V, Murray TM,Hodsman AB, Robert NJ, Sutton RAL: Regional migratory osteoporosis of the lower extremities with vertebral osteoporosis. Bone 7:343 – 349, 1986.
25. Wamneck N, Munk PJ, Lee MJ, Meek RN: Intra-articular regional migratory osteoporosis of the knee. Skeletal Radiol 29: 97 – 100, 2000.
26. Levy D, Hinterbuckner C: Transient or migratory osteoporosis of lower extremity. NY State J Med 76: 739 – 742, 1976.
27. Veldman PH, Reynan HM, Arntz IE, Goris RJ: Signs and symptoms of reflex sympathetic dystrophy: Prospective study of 829 patients. Lancet 342: 1012 – 1016, 1993.
28. Fialka V: The diagnosis of reflex sympathetic dystrophy. Eur J Phys Med Rehab 2: 40 – 44, 1992.
29. Geurra JJ, Steinberg ME: Distinguishing transient osteoporosis from avascular necrosis of the hip. J Bone Joint Surg 77A: 616 – 624, 1995.
30. Tannenbaum H, Esdaile J, Rosenthall L: Joint imaging in regional migratory osteoporosis. J Rheumatol 7: 237 – 244, 1980.
31. Gupta RC, Popovtzer MM, Huffer WE, Smyth CJ: Regional migratory osteoporosis. Arthritis Rheum 16: 363 – 368, 1973.
32. Shifrin LZ, Reis ND, Zinman H, Besser MI: Idiopathic transient osteoporosis of the hip. J Bone Joint Surg 69B: 769 – 773, 1987.
33. Trevisan C, Ortolani S: Bone loss and recovery in Regional Migratory Osteoporosis. Osteoporosis Int 13: 901 – 906, 2002.
34. Renier JC, Basle M, Masson C, Bregon C, Audran M: Migratory algodystrophy of the lower limbs involving the foot and complicated by two fatigue fractures: an histological bone study. Rev Rheum. Ed Fr 60: 469 – 473, 1993.
35. Schapira D, Gutierrez G, Mor M, Nahir AM: Successful pamidronate treatment of severe and refractory regional migratory osteoporosis. J Clin Rheumatol 7 (3):188 – 190, 2001.
36. DeBastiani G, Nogarin L, Perusi M: Pig calcitonin in the treatment of localised osteoporosis. Ital J Orthop Traumatol 2:18, 1976.
37. Doury P, Delahayer RP, Granier R, Pattin S, Metges PJ: Highly localised transient osteoporosis of the knee. Arthritis Rheum 21: 992 – 993, 1978.
38. Lagier R: Partial algodystrophy of the knee: An anatomicroradiological study of one case. J Rheumatol 10: 255 – 260, 1983..
39. Naides SJ, Resnick D, Zvaifler NJ: Idiopathic regional osteoporosis: A clinical spectrum. J Rheumatol 12:763 – 768, 1985.
40. Jacox RF, Waterhouse C, Taves DR: Transient painful osteolysis: A metabolic study. J Rheumatol 2: 279 – 283, 1982
41. Fingeroth RJ: Successful operative treatment of a displaced subcapital fracture of the hip in transient osteoporosis of pregnancy. A case report and review of the literature. J Bone Joint Surg 77A: 127 – 131, 1995.
42. Fokler SK, Vengust V: Displaced subcapital fracture of the hip in transient osteoporosis of pregnancy. Int Orthop 21: 201 – 203, 1997.
43. Carty S, Herdman G, Williams F, Srinavasan U: Transient migratory osteoporosis: rapid response to pamidronate treatment. J Clin Rheumatol 13: 138 – 139, 2007.

Address correspondence to: Simon B.M. MacLean, Orthopaedic Department,
New Cross Hospital, Wolverhampton. WV10 OQP
Email: simon_maclean81@hotmail.com
Tel: +447866 766 271

1,2,3,4,5,6   Orthopaedic Department, New Cross Hospital, Wolverhampton.

© The Foot and Ankle Online Journal, 2009

Pure Tibiotalar Dislocation with Talus Bone Contusion in a Volleyball Player: A case report

by N.E. Koukoulias, MD, PhD1 , S.G. Papastergiou, MD, PhD2, P. Panagopoulos, MD3, T. Dimitriadis, MD4, P. Koumis, MD5

The Foot and Ankle Online Journal 2 (9): 2

We present a case of closed, pure tibiotalar dislocation. A 21 year-old volleyball player sustained a pure ankle dislocation after jumping up at the net and landing on the floor with a fully plantarflexed foot that was inverted during landing. After closed reduction, a short leg cast was applied for ankle immobilization. Magnetic resonance imaging demonstrated rupture of the anterolateral capsuloligamentous structures and talus bone contusion. The cast was removed at two months post-injury and full weight-bearing was permitted at three months. The patient returned to pre-injury level of activity at 6 months. Three years post-injury, the patient is asymptomatic, without signs of instability or degenerative arthritis.

Key words: Tibiotalar dislocation, talus contusion, magnetic resonance imaging.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot and Ankle Online Journal (www.faoj.org)

Accepted: August, 2009
Published: September, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0209.0002

Closed tibiotalar dislocation without concomitant malleolar fracture or syndesmotic injury is a rare. [1-5] Ankle sprain is often accompanied by chondral or osteochondral injuries that may result in persisted pain and disability. [6,7]

This is the first case of pure ankle dislocation in the literature, with documented talus bone contusion. This finding is crucial for proper treatment planning in order to avoid complications like tibiotalar degenerative arthritis and talar avascular necrosis.

Case Report

A 21 year-old volleyball player injured his left ankle during a second league game. The injury occurred after jumping up at the net and landing on the floor with a fully plantarflexed foot that was inverted during landing. (Fig. 1)

Figure 1 The anteroposterior view demonstrates tibiotalar joint dislocation without concomitant malleolar fracture or syndesmotic injury.

Physical examination in the emergency room showed a deformed ankle without neurovascular deficit of the foot. Radiographs of the ankle demonstrated ankle dislocation without concomitant syndesmotic injury or malleolar fracture.

The ankle was reduced under general anaesthesia. After close reduction, a short leg cast was used for ankle immobilization. (Fig. 2) The patient was then further investigated with magnetic resonance imaging (MRI) to fully explore the structures that were injured. MRI demonstrated rupture of the anterior capsule and anterior talo-fibular ligament and talus bone contusion. (Fig. 3) The cast was kept on for two months. After the cast removal, the patient was referred to the physiotherapist and range of motion exercises were initiated along with partial weight-bearing. Three months post-injury, full weight-bearing was permitted.

Figure 2 Lateral view of the tibiotalar joint after closed reduction.

Figure 3 T1 sagittal image demonstrates talus bone contusion.

The patient returned to the pre-injury level of activity at six months post-injury. At physical examination there were no signs of residual ligamentous laxity and no ankle effusion and tenderness. Three years post-injury the patient is still asymptomatic without signs of tibiotalar degenerative arthritis or talar avascular necrosis in ankle radiographs.


In 1939, Wilson, et al., were the first to report on ankle dislocation without fracture. Since this time, closed pure ankle dislocations were sporadically reported, while other authors reported open dislocations or dislocations accompanied by tibio-fibular diastasis (syndesmotic injury) or mixed data. [1-5]

Interestingly, none of these cases was investigated with MRI. All patients had conventional radiography that, generally, cannot reveal chondral or osteochondral injuries.6 In comparison, MRI is a high sensitive modality for detecting this kind of pathology. [6] Sijbrandij, et al., found chondral and osteochondral injuries in 18% of their patients with ankle sprain. [6] Ly and Fallat reported that these injuries are responsible for persisted pain and disability after ankle sprain. [7] It is assumed that incidence and degree of bone contusion depends on the severity of the sprain and the residual instability that could cause recurrent sprains. [6] The natural history of ankle bone contusion is still unknown. The evolution towards tibiotalar degenerative arthritis or talar avascular necrosis has not been extensively studied in the literature.

Sijbrandij, et al., found that bone contusion was resolved in 1 – 4 months after injury, but in some cases persisted for more than 4 months. [6] In contrast, degenerative arthritis after ankle dislocation should be anticipated in 25% of cases.5 As a result, MRI is mandatory for accurate diagnosis and proper treatment planning in these severe injuries.

Most of the authors reported on ankle dislocation without fracture, recommend conservative treatment using a short leg cast for 4 – 6 weeks and full weight bearing at 3 – 6 weeks. Nevertheless, only Tayamaz and Gunal reported long-term results of their case. [4] Consequently, no safe conclusions can be drawn regarding the success of the treatment. In our opinion, these cases should be treated individually, based primarily on an accurate diagnosis provided by MRI. The length of immobilization should be 6 – 8 weeks to allow soft tissue healing. Full weight-bearing should be decided according to the presence and degree of chondral and osteochondral injury in combination with joint effusion and tenderness assessed in physical examination. It is clear that long-term follow up studies are needed to establish treatment guidelines for these severe injuries.


1. Wilson MJ, Michele AA, Jacobson EW: Ankle dislocations without fracture. J Bone Joint Surg 21A: 198 – 204, 1939.
2. Uyar M, Tan A, Işler M, Cetinus E: Closed posteromedial dislocation of the tibiotalar joint without fracture in a basketball player. Br J Sports Med 38 (3):342 – 343, 2004.
3. Soyer AD, Nestor BJ, Friedman SJ: Closed posteromedial dislocation of the tibiotalar joint without fracture or diastasis: a case report. Foot Ankle Int 15 (11):622 – 624, 1994.
4. Taymaz A, Gunal I: Complete dislocation of the talus unaccompanied by fracture. J Foot Ankle Surg 44 (2):156 – 158, 2005.
5. Elisé S, Maynou C, Mestdagh H, Forgeois P, Labourdette P: Simple tibiotalar luxation. A proposal of 16 cases. Acta Orthop Belg 64 (1):25 – 34, 1998.
6. Sijbrandij ES, van Gils AP, Louwerens JW, de Lange EE: Posttraumatic subchondral bone contusions and fractures of the talotibial joint: occurrence of “kissing” lesions. Am J Roentgenol 175 (6):1707 – 1710, 2000.
7. Ly PN, Fallat M: Transchondral contusions of the talus: a review of 64 surgical cases. J Foot Surg 32 (4):352 – 374, 1993.

Address correspondence to: N.E. Koukoulias, 161 Ethnikis Antistasis St, 55134, Thessaloniki, Greece, Tel: 00302310493552.

1,2,3,4,5  Department of Orthopaedics, Sports Injuries Unit, “Agios Pavlos” General Hospital, Thessaloniki, Greece.

© The Foot and Ankle Online Journal, 2009

Plantar Fascial Rupture of the Foot: A case report

by Al Kline, DPM1  

The Foot and Ankle Online Journal 2 (5): 4

Plantar fascial rupture is rarely presented in the literature. Spontaneous rupture of the plantar fascia is commonly preceded by plantar fasciitis. A 60 year old male presents following an acute injury of his foot while playing softball. He presents with acute pain and ecchymosis to the plantar arch of the foot. Plantar fascial rupture was diagnosed clinically and confirmed on magnetic resonance imaging (MRI). This case discusses the clinical evaluation, MRI results and treatment of acute, spontaneous rupture of the plantar fascia. We also describe the MRI differences of plantar fasciitis and plantar fascial rupture.

Key words: Plantar fasciitis, plantar fascial rupture, heel pain, Magnetic resonance imaging

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot and Ankle Online Journal (www.faoj.org)

Accepted: April, 2007
Published: May, 2009

Plantar fascial injuries are a common source of foot pain. Plantar fasciitis is the most common type of plantar fascial injury. The condition is characterized by small tears of the plantar aponeurosis that can cause inflammation and thickening of the plantar aponeurosis. The causes of injury are related most commonly to stress and strain. General injury to the plantar fascia can be divided into three categories: mechanical, degenerative and systemic. [1] Mechanical conditions such as pronation, forefoot varus and rearfoot valgus will often lead to increased tension and strain of the plantar aponeurosis. This may be exacerabated by increased activity and lack of proper shoe and in-step support. It is now widely accepted that degenerative changes can occur within the plantar fascia due to repetitive micro tears and peri-fascial edema termed plantar fasciosis. [2] This is characterized as a degenerative process of myxoid degeneration without inflammation. [2]

There are also a number of inflammatory systemic conditions that can cause plantar fasciitis. These include rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, Reiter’s syndrome, gout, Behcet’s Syndrome and systemic lupus erythematosus.3 In general, the etiology of arch and heel pain can be mulifactorial in nature. When tension along the plantar aponeurosis exceeds its inherent strength, an acute fascial rupture can result.

Case Report

A 60-year old healthy male presented to our office in acute pain. He presented with a limp. He stated that he had been having arch and heel pain of the right foot over the past month. He recently participated in a softball game. He states that while ‘sprinting’ to a base, he felt a ‘pop’ in his arch followed by acute pain and swelling. He immediately stopped playing and placed ice on the arch region of the foot. Clinical evaluation of the foot reveals an extremely tender plantar fascia with localized bruising or ecchymosis (Fig.1).

Figure 1  The plantar fascia shows bruising directly along the arch of the foot.  There is extreme point tenderness to this region.

Pain was palpable along the entire course of the plantar fascia and more pronounced along the central arch. The patient was sent for magnetic resonance imaging (MRI) confirmation to rule out plantar fascial rupture. Pain was palpable along the entire course of the plantar fascia and more pronounced along the central arch. The patient was sent for MRI confirmation to rule out plantar fascial rupture.

MR Imaging and Findings

MRI shows classic signs of fascial tear and rupture. Multiplanar, multisequence images were obtained showing increased thickness of the plantar fascia up to 10mm with convexed dorsal thickening. A classic fusiform appearance of the fascia is seen in the region of rupture.

The sagittal image also shows intrafascial high signal echo on T2 imaging consistent with plantar fascial disruption of the fibers. (Fig. 2)

Perifascial edema (arrow) is seen along the deeper musculature adjacent to the plantar aponeurosis. The coronal view on STIR or inversion recovery sequencing shows dramatic intrafascial edema and hemorrhage. Again, fusiform thickening of the musculature and plantar aponeurosis is appreciated. (Fig. 3)

Figure 2  T2 sagittal image shows a central thickening up to 10mm with enlargement and nodular thickening of the plantar aponeurosis.

Figure 3  STIR (inversion recovery image) coronal views also shows intrafascial edema and hemorrhage.

Axial imaging shows increased signal intensity on T1 and T2 imaging with appreciable intrafascial and perifascial edema. (Fig. 4 A and B)


Figure 4A and 4B  MR Axial imaging shows T1 image (A).  The T2 image shows increased perifascial, intrafascial and muscular edema. (B)


Treatment of plantar fascia rupture depends on the extent of injury confirmed by MRI findings and activity level of the patient. Our patient was active for his age and his overall injury was acute and extremely painful. In this respect, we recommended the patient wear a non-weight bearing cast for 4 weeks.

We placed him on NSAIDS for 2 weeks during his casting period. His recovery after casting included local stretching and physical therapy. We also placed him in orthotics.


The clinical presentation of acute plantar fascial rupture differs from plantar fasciitis. The pain of an acute rupture is located more distal to the insertion of the plantar fascia and bruising is commonly seen along the middle of the arch. Clinically, this is extremely tender to touch and the patient will have trouble walking. Most often, clinical evaluation, activity of the patient and onset of pain will help the practitioner determine the extent of injury and determine fascial strain or fasciitis from actual tear or rupture of the plantar fascia. Radiographic evaluation lacks the proper contrast resolution for proper differentiation of plantar fasciitis and fascial rupture. Fascial thickening and perifascial edema can be seen on enhanced soft tissue radiographic imaging. However, MR imaging is superior in differentiating acute plantar fasciitis, chronic plantar fasciitis from partial or acute plantar fascial rupture. MR imaging will determine the exact localization and extent of fascial injury. In this regard, the proportionate thickness and amount of edema will help the practitioner determine the proper course of treatment.

The attachment of the plantar fascia is best demonstrated on coronal images. The entire course of the aponeurosis is best seen on the sagittal images. Visualizing of the medial fascial band is best seen in the sagittal and coronal views. The lateral band is best observed with oblique imaging, although sagittal and coronal images can also be used. MR imaging studies also show a difference in findings when comparing fasciitis and fascial rupture. In plantar fasciitis, there is often thickening of the aponeurosis as seen on sagittal image without actual disruption of the fascial fibers. The appearance of the plantar fascia is usually thickened and uniform. In plantar fascial rupture, there is often a fusiform appearance of the aponeurosis.

There is also widespread abnormal high signal intensity infiltrating perifascial soft tissues consistent with local edema. The most consistent finding in acute partial or complete rupture of the plantar aponeurosis is fusiform thickening of the fascia with abnormal, intrafascial signal intensity. Theodorou, et al., studied MR imaging of 14 patients with partial or complete rupture of the plantar fascia revealing abnormal, fusiform thickening of the plantar aponeurosis in all patients. All patients showed abnormal absence of T1-weighted low signal intensity of the plantar aponeurosis at the site of complete rupture or partial loss of T1-weighted low signal intensity respectively. [1]

Treatment can vary on extent of injury and activity of the patient. In earlier studies and before MR imaging techniques, patients with rupture were often treated conservatively using crutches, ice packs, anti-inflammatory agents and foot straps. Diagnosis was simply made by presentation of acute symptoms such as severe localized swelling and acute tenderness. As the swelling diminished, there is often a palpable defect that is replaced by a hard mass that gradually became less tender. [4] Leach, et al., reported suspected partial ruptures in six long distance runners who were treated conservatively. Only one patient required surgery for persistent swelling, undergoing a fascial release. They reported full recovery of all the long distance runners back to their original pre-injury activity with no deleterious effects, even in the one surgical patient. Now, with the aid of MR imaging, diagnosis and treatment can be more specific to extent of injury.

This case highlights clinical and MRI findings in a patient with plantar fascial rupture following an acute injury while playing softball. A fusiform appearance of the fascia on MR imaging was consistent with plantar fascial rupture and the patient’s clinical presentation. In its largest point, the intrafascial edema can increase the thickness of the fascia to over 10 mm. The normal thickness of the plantar fascia is about 4 mm in thickness. In cases of plantar fasciitis, the thickness can increase to 8mm. Most fascial ruptures and partial tears show an increase in thickness of the fascia of 10mm or more with intrafascial high signal intensity of T2 weighted MR images.

In plantar fasciitis, the MR T2 weighted imaging or bright signal intensity is not actually seen within the fascia, but can be readily seen perifascially. If a bright signal is seen within the fascia, it will represent rupture of the fascial fibers confirming the diagnosis of plantar fascial rupture.


1. Theodorou, D.J., et al.: Plantar fasciitis and fascial rupture: MR imaging findings in 26 patients supplemented with anatomic data in cadavers. Radiographics. 20: S181- S197, 2000.
2. Lemont H, Ammirati, KM, Usen N: Plantar fasciitis: A degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc 93(3): 234 – 237, 2003.
3. Barrett SL, O’Malley R.: Plantar fasciitis and other causes of heel pain. American Family Physician 59 (8), 1999.
4. Leach R, Jones R, Silva T: Rupture of the plantar fascia in athletes. J Bone Joint Surgery 60A (4): 537 – 539, 1978.

Address correspondence to: Al Kline, DPM
3130 South Alameda, Corpus Christi, Texas 78404.

1 Adjunct Clinical Faculty, Barry University School of Podiatric Medicine. Private practice, Chief of Podiatry, Doctors Regional Medical Center. Corpus Christi, Texas, 78411.

© The Foot and Ankle Online Journal, 2009