(Radiographics. 2000;20:S279-S293.)
© RSNA, 2000
Multiregional Pathologic Processes |
Neuropathic Osteoarthropathy: Diagnostic Dilemmas and Differential Diagnosis1
Elizabeth A. Jones, MD, 2,
B. J. Manaster, MD, PhD, 3,
David A. May, MD and
David G. Disler, MD
1 From the Department of Radiology, Medical College of Virginia of Virginia Commonwealth University, 401 N 12th St, PO Box 980615, Richmond, VA 23298-0615. Presented as a scientific exhibit at the 1999 RSNA scientific assembly. Received February 16, 2000; revision requested April 12 and received May 8; accepted May 12. Address correspondence to E.A.J. (e-mail:bethanne@firstworld.net).
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Abstract
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The purpose of this pictorial essay is to illustrate the radiologic spectrum of imaging findings of neuropathic osteoarthropathy. Typical findings include joint destruction, disorganization, and effusion with osseous debris. A variety of other imaging findings related to neuropathic osteoarthropathy such as resorption of the ends of tubular bones and neuropathic fracture are shown. The two prevailing theories for the pathophysiology of neuropathic bone and joint disease, the neurovascular and neurotraumatic theories, are briefly described. Examples of osteoarthropathy from diverse causes are presented including syringomyelia, spinal cord injury, meningomyelocele, diabetes mellitus, congenital insensitivity to pain, steroid injections, syphilis, leprosy, and others. The discussion focuses on key imaging features with emphasis on disease patterns and differential diagnosis, which vary by skeletal location.
Index Terms: Bones, neuropathic disorder, 40.821
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- Recognize the radiologic manifestations of neuropathic osteoarthropathy.
- List other diseases that may be confused with neuropathic osteoarthropathy.
- Describe the differential diagnosis of neuropathic osteoarthropathy with emphasis on skeletal location.
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Introduction
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Neuropathic osteoarthropathy represents a spectrum of bone and joint destructive processes associated with neurosensory deficit. Loss of proprioception has been implicated as a causative factor in pathogenesis of the disease. Patients with diabetes mellitus, syringomyelia, syphilis, and other neuropathies are prone to this disease. Sensory deficits may arise in the spinal cord or in peripheral nerves. Correct radiologic diagnosis is important, because the underlying cause for the bone and joint disorder might otherwise go undetected and the radiologic findings could be confused with osteoarthritis, infection, or tumor. In this article, we list possible causes of neuropathic osteoarthropathy (Table), briefly discuss the two major theories for the pathophysiology of the disease, and describe the radiologic patterns encountered. Clinical dilemmas and additional radiologic details specific to skeletal location are then discussed.
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Background
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The relationship between neuropathic arthropathies and central nervous system lesions was elucidated by Jean Martin Charcot in 1868 (1). Charcot believed that the disease resulted from damage to central nervous system trophic centers that controlled bone and joint nutrition. Although the Charcot theory is no longer accepted, joints affected by the disorder are still often referred to as Charcot joints. Today, two main theories for the pathophysiology of neuropathic arthropathy are proposed.
The neurotraumatic theory holds that in the absence of normal protective sensory feedback, repetitive mechanical trauma causes progressive joint destruction. This theory is supported by experiments performed by Eloesser (2) in the early 1900s in which he produced anesthesia in the limbs of animals by severing the posterior nerve roots and showed that sensory loss in and of itself did not result in arthropathy. When the anesthetized joints were subjected to trauma, however, typical neuropathic joint lesions occurred.
Others (3–6) support a neurovascular theory, which emphasizes the vascular changes that accompany neuropathic arthropathy. Studies have shown that in the absence of a neural stimulus in the limb, sympathetic tone to the limb is lost with resultant vasodilation and hyperemia, which in turn promote bone resorption. Weakened subchondral bone thus results in neuropathic changes.
Both the neurotraumatic and neurovascular theories are supported by clinical and laboratory
data. For example, it is well known that neuropathic osteoarthropathy may occur in immobilized patients. In these cases, minor trauma inflicted during patient transport, turning in bed, or passive exercise is superimposed on bone weakened by neurovascular mechanisms and is thought to be responsible (7).
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Radiologic Patterns
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Both hypertrophic and atrophic patterns of neuropathic osteoarthropathy are depicted radiologically. The classically described hypertrophic joint is manifested radiologically as joint destruction and fragmentation, osseous sclerosis, and osteophyte formation. Osteophytes formed in the setting of neuropathic arthropathy may differ from those of osteoarthritis on the basis of early production of ill-defined and rounded margins and later attainment of enormous size. In many cases, however, it is difficult to distinguish neuropathic osteoarthropathy from severe osteoarthritis.
The atrophic form of neuropathic osteoarthropathy has an appearance of osseous resorption that often gives the impression of surgical amputation. Joint disorganization and large persistent bloody joint effusion are features of both atrophic and hypertrophic types of neuropathic osteoarthropathy, and, when severe, both types exhibit disorganization more profound than that seen in other forms of arthropathy. Milder degrees of the disease, however, may be difficult to diagnose.
The atrophic type may appear similar to septic arthritis, and the hypertrophic type, as mentioned earlier, may appear similar to osteoarthritis. The completely resorbed atrophic joint is more common than is the purely productive hypertrophic joint, and mixed patterns are frequently encountered. The atrophic pattern is more common in the non–weight-bearing joints of the upper extremity and is associated with syringomyelia and peripheral nerve lesions. Either pattern may be seen with central or peripheral neurosensory deficit, however, and in some cases an affected joint may exhibit the atrophic pattern early and evolve into the hypertrophic form later.
Fractures are an important although less well-known manifestation of neuropathic osteoarthropathy. These fractures may occur spontaneously or in the presence of minor trauma. In long bones, they are typically transverse in orientation. These fractures are often initially unrecognized and, in the setting of delayed treatment with continued weight bearing and motion at the fracture site, may heal with exuberant and bizarre callus formation (8).
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Upper Extremity
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Neuropathic osteoarthropathy in the non–weight-bearing joints of the upper extremity is relatively rare compared with that in the lower extremity. The most common cause of a neuropathic shoulder is syringomyelia. The discovery of neuropathic arthropathy of the upper extremity in the absence of a known spinal cord lesion should prompt imaging of the cervical cord. A syrinx may be due to an intrinsic central cord lesion, or it may develop as a consequence of cord trauma in patients with paraplegia (9).
In the shoulder, patients may present clinically with a shoulder mass due to fluid distention of the glenohumeral joint and the subacromial-subdeltoid bursa. Osseous fragmentation and debris, a hallmark of neuropathic osteoarthropathy, may be confused with tumor matrix on radiographs. Not uncommonly, a neuropathic shoulder is initially misdiagnosed radiographically as a neoplasm, particularly as chondrosarcoma. Imaging features that help differentiate soft-tissue tumors from neuropathic arthropathy of the shoulder include an amputated appearance of the proximal humerus, dislocation, large joint effusion, and fragmented osseous debris. Osseous fragments often line the distended joint capsule and reside in the subacromial-subdeltoid bursa. Most important, the abnormality is centered at the joint with osseous involvement on both sides of the joint. Bone tumors, on the other hand, localize to bone on one side of the joint and only rarely violate cartilage boundaries (Figs 1–3).
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Figure 1a. Neuropathic osteoarthropathy of the shoulder in a 45-year-old man with a syrinx. (a) Frontal (anteroposterior) radiograph depicts osteolysis resembling amputation with sharply circumscribed margins. Normal mineralization is maintained in the remaining humerus. Debris lines the distended joint capsule, subscapular recess (black arrow), and axillary recess (white arrow). (b) T1-weighted spin-echo magnetic resonance (MR) image (repetition time msec/echo time msec = 500/20) of the cervical spine helps confirm the presence of a syrinx (arrows). (From the American College of Radiology [ACR] Learning File, MSK case 235.)
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Figure 1b. Neuropathic osteoarthropathy of the shoulder in a 45-year-old man with a syrinx. (a) Frontal (anteroposterior) radiograph depicts osteolysis resembling amputation with sharply circumscribed margins. Normal mineralization is maintained in the remaining humerus. Debris lines the distended joint capsule, subscapular recess (black arrow), and axillary recess (white arrow). (b) T1-weighted spin-echo magnetic resonance (MR) image (repetition time msec/echo time msec = 500/20) of the cervical spine helps confirm the presence of a syrinx (arrows). (From the American College of Radiology [ACR] Learning File, MSK case 235.)
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Figure 2a. Initial diagnosis of chondrosarcoma in a 76-year-old woman was found to be a neuropathic shoulder. (a) Frontal radiograph depicts classic findings of neuropathic arthropathy, including destruction of the humeral head that resembles amputation (arrowheads), dislocation, and debris (arrow). (b) T2-weighted spin-echo MR image (2,550/96) shows a large joint effusion and ossific debris (arrow) residing in the fluid-filled joint rather than arising in the soft-tissue tumor. (c) CT scan shows debris lining the distended joint capsule (arrows). The patient was found to have a syrinx (not shown).
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Figure 2b. Initial diagnosis of chondrosarcoma in a 76-year-old woman was found to be a neuropathic shoulder. (a) Frontal radiograph depicts classic findings of neuropathic arthropathy, including destruction of the humeral head that resembles amputation (arrowheads), dislocation, and debris (arrow). (b) T2-weighted spin-echo MR image (2,550/96) shows a large joint effusion and ossific debris (arrow) residing in the fluid-filled joint rather than arising in the soft-tissue tumor. (c) CT scan shows debris lining the distended joint capsule (arrows). The patient was found to have a syrinx (not shown).
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Figure 2c. Initial diagnosis of chondrosarcoma in a 76-year-old woman was found to be a neuropathic shoulder. (a) Frontal radiograph depicts classic findings of neuropathic arthropathy, including destruction of the humeral head that resembles amputation (arrowheads), dislocation, and debris (arrow). (b) T2-weighted spin-echo MR image (2,550/96) shows a large joint effusion and ossific debris (arrow) residing in the fluid-filled joint rather than arising in the soft-tissue tumor. (c) CT scan shows debris lining the distended joint capsule (arrows). The patient was found to have a syrinx (not shown).
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Figure 3a. Neuropathic osteoarthropathy of the shoulder in a 28-year-old patient with paraplegia below T8. (a) Chest radiograph shows asymptomatic destruction of the left glenohumeral joint (solid arrow). Note spinal fixation hardware (open arrows). (b) Axial CT scan shows osseous debris (arrowheads) lining a joint distended by hypoattenuating fluid. (c) T2-weighted spin-echo MR image (2,400/80) of the cervical spine reveals an extensive syrinx.
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Figure 3b. Neuropathic osteoarthropathy of the shoulder in a 28-year-old patient with paraplegia below T8. (a) Chest radiograph shows asymptomatic destruction of the left glenohumeral joint (solid arrow). Note spinal fixation hardware (open arrows). (b) Axial CT scan shows osseous debris (arrowheads) lining a joint distended by hypoattenuating fluid. (c) T2-weighted spin-echo MR image (2,400/80) of the cervical spine reveals an extensive syrinx.
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Figure 3c. Neuropathic osteoarthropathy of the shoulder in a 28-year-old patient with paraplegia below T8. (a) Chest radiograph shows asymptomatic destruction of the left glenohumeral joint (solid arrow). Note spinal fixation hardware (open arrows). (b) Axial CT scan shows osseous debris (arrowheads) lining a joint distended by hypoattenuating fluid. (c) T2-weighted spin-echo MR image (2,400/80) of the cervical spine reveals an extensive syrinx.
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Neuropathic arthropathy in non–weight-bearing joints of the upper extremity has also been described in leprosy and occasionally in patients with diabetes mellitus. Leprosy (Hansen disease) is an uncommon condition in the United States. Mycobacterium leprae attacks the skin and peripheral nerves and has a predilection for the cooler appendages of the body with characteristic involvement of the small bones of the hands and feet. Bone lesions due to direct leprous infection are unusual, varying from 3% to 5% in one series (10), and these lesions exhibit radiologic findings of acute and chronic osteomyelitis similar to those of other granulomatous infectious agents. Bone lesions in patients with leprosy are usually due to trauma and secondary bacterial infection superimposed on denervated tissues (11). The radiologic findings are similar to those caused by other conditions in which sensory impairment is complicated by traumatic injury and infection such as diabetes mellitus, frostbite, pernicious anemia, scleroderma, syringomyelia, tabes dorsalis, and familial sensory neuropathy.
Motor denervation due to leprous infection of peripheral nerves contributes to deformities such as claw hand and claw toes and is sometimes associated with the development of concentric bone atrophy. The development of concentric bone resorption is not fully understood but is thought to occur in the active paralytic extremity owing to an imbalance between tensile and compressive forces that maintain normal bone architecture (11). Absorption of bone in leprosy manifests as a decrease in bone length and width and results in a tapered appearance at the end of the bone, which has been likened to a licked candy stick. When complicated by repeated
microtrauma, secondary bacterial infection, or both, digits may be resorbed (Fig 4).
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Figure 4. Frontal radiograph depicts the hand of a 42-year-old man with leprosy. "Amputations" and deformities are most often due to trauma and infection in insensate hands. The distal phalanx of the thumb has a configuration resembling a licked candy stick (arrow) that is sometimes seen in neuropathic osteoarthropathy of digits.
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Spine
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Neuropathic osteoarthropathy of the spine may occur in isolation or in combination with neuropathic osteoarthropathy of other joints. The thoracolumbar junction and lumbar spine are most frequently affected, and one or more vertebral segments may be involved. Radiologically, findings of either sclerosis or osteolysis may predominate. Indeed, the spinal changes are often initially thought to be due to vertebral osteomyelitis or metastatic destruction of a vertebra. Radiographs of the spine may show disc space narrowing, vertebral lysis or sclerosis, subluxations, abrupt curvature, and often paraspinal soft-tissue calcifications. Large hypertrophic end-plate osteophytes may form. Computed tomographic (CT) changes of neuropathic osteoarthropathy of the spine are those of sclerosis and destruction of all three vertebral columns including destruction of the facet joints and can be important in distinguishing neuropathic osteoarthropathy from vertebral osteomyelitis, which typically involves a single vertebral column (12).
Osseous fragments typically extend beyond the confines of the vertebral body margins into paraspinous and erector spinae musculature and into the spinal canal (13). Bone debris and effusion may result in a paraspinous mass containing calcifications, but a large enhancing solid paraspinous or epidural mass is typically lacking. The presence of vertebral body sclerosis and osseous fragmentation are further imaging findings that help differentiate neuropathic spine from other processes. Sclerosis and osseous destruction in vertebral osteomyelitis are typically limited to the adjacent end plates. Extensive osseous fragmentation is not an expected imaging finding in typical bacterial vertebral osteomyelitis or metastatic disease of the spine. Granulomatous infection of the spine may result in calcifications in the paraspinous soft tissues and may simulate axial neuropathic osteoarthropathy; however, fragmentation of the facet joints would not be expected. The usual causes of axial neuropathic osteoarthropathy are traumatic spinal cord injury, inadequately treated syphilis, amyloidosis, congenital insensitivity to pain, and occasionally diabetes mellitus (Fig 5).
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Figure 5a. Axial neuropathic osteoarthropathy in a 66-year-old diabetic woman. (a) Lateral radiograph of the lumbar spine shows destruction (arrow) and posterior subluxation of T12. (b) Axial CT scan of T12 vertebra shows osseous debris in the spinal canal (solid arrow), fragmentation of posterior elements (open arrows), and an "exploded" appearance, findings that suggest a neuropathic cause. Multiple biopsy samples failed to reveal infection or tumor.
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Figure 5b. Axial neuropathic osteoarthropathy in a 66-year-old diabetic woman. (a) Lateral radiograph of the lumbar spine shows destruction (arrow) and posterior subluxation of T12. (b) Axial CT scan of T12 vertebra shows osseous debris in the spinal canal (solid arrow), fragmentation of posterior elements (open arrows), and an "exploded" appearance, findings that suggest a neuropathic cause. Multiple biopsy samples failed to reveal infection or tumor.
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In the setting of posttraumatic paraplegia or quadriplegia, neuropathic osteoarthropathy may occur in vertebrae distal to the level of spinal cord injury, and severe spinal deformity and gross instability may develop (Fig 6). Such patients often have neurogenic bladders and are at substantial risk for disk space infection because of the rich venous drainage of the pelvis along the spinal venous plexus. Since imaging findings often simulate vertebral osteomyelitis of bacterial or granulomatous origin, disk aspiration is often preferable to exclude infection, although, if properly recognized as neuropathic osteoarthropathy, may be unnecessary. In paraplegics who have previously undergone a spinal fusion procedure, neuropathic changes typically develop in the first mobile spinal segment below the caudal end of the fusion (14) (Fig 7).
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Figure 6a. Neuropathic spine in a 45-year-old man with chronic quadriplegia below C6 and new long-tract signs. (a) Lateral radiograph depicts destructive changes of T7 through T9 vertebral bodies, with subluxation, end-plate destruction (arrowheads), sclerosis (arrows), and osteophyte formation. (b) Sagittal T2-weighted spin-echo MR image (4,000/96) shows a retropulsed vertebral body (arrow) with epidural encroachment on the spinal cord; however, there is no paravertebral mass or epidural abscess.
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Figure 6b. Neuropathic spine in a 45-year-old man with chronic quadriplegia below C6 and new long-tract signs. (a) Lateral radiograph depicts destructive changes of T7 through T9 vertebral bodies, with subluxation, end-plate destruction (arrowheads), sclerosis (arrows), and osteophyte formation. (b) Sagittal T2-weighted spin-echo MR image (4,000/96) shows a retropulsed vertebral body (arrow) with epidural encroachment on the spinal cord; however, there is no paravertebral mass or epidural abscess.
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Figure 7. Lateral radiograph depicts a neuropathic spine in a 36-year-old male paraplegic with a remote history of a burst fracture of L1 treated with partial corpectomy and placement of a strut graft (black arrow) and posterior spinal rods. Destruction of end plates at L3-4, L4-5, and L5-S1 (white arrows) is seen. Increased density in L3 through L5 vertebral bodies favors diagnosis of neuropathic osteoarthropathy.
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Lower Extremity
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Neuropathic osteoarthropathy is observed much more frequently in the lower extremity than in the upper extremity. In the past, syphilis was the most common cause of neuropathic osteoarthropathy and most commonly affected the knee (Figs 8, 9). Today, diabetes mellitus is the most common cause, and neuropathic osteoarthropathy in this setting most often affects the foot and ankle. It usually occurs with long-term, poorly controlled diabetes. There are reports, however, in which the osteoarthropathy was the presenting symptom of the disease (15). Although joint changes in the absence of reported trauma is typical, neuropathic changes in the feet of diabetic patients may be precipitated by minor trauma. Soft-tissue swelling, warmth, and erythema are seen clinically in the early stages, usually with decreased but not absent pain sensation. Neuropathic osteoarthropathy in the diabetic foot often begins in the midfoot, and subluxation usually starts at the second tarsometatarsal joint and proceeds laterally (16).
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Figure 8. Frontal radiograph depicts neuropathic osteoarthropathy of the knee in a 50-year-old man with tertiary syphilis. Tibial plateaus are impacted and fragmented (black arrows). Bone fragments dissected down the medial calf (white arrow) are faintly seen. Such fragments can dissect in fascial planes to reside far from the joint. (From the ACR Learning File, MSK case 234.)
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Figure 9. Frontal radiograph depicts pronounced neuropathic osteoarthropathy of the knees in a 68-year-old man with long-term neurosyphilis. The distal femurs are deformed and shaped like a chicken drumstick. The tibias are laterally subluxated with valgus angulation. Marked periarticular osseous debris is present. In patients with syphilis, osteoarthropathy most commonly affects the knee.
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Any patient with a Lisfranc fracture, or dislocation in the absence of acute trauma, should undergo evaluation for diabetes mellitus and other causes of sensory neuropathy (17) (Figs 10–13). Atrophic neuropathic arthropathy of the foot, especially associated with vascular calcifications, is highly suggestive of diabetes mellitus. However, both atrophic and hypertrophic joints are seen in diabetic patients (Fig 14). The ankle, hindfoot, and forefoot may also show neuropathic changes (Figs 15–22). Neuropathic fractures that are well known to occur in the diabetic foot are avulsion fractures of the posterior tubercle of the calcaneus and subchondral fracture of the head of the second metatarsal (similar to Freiberg infraction) (19) (Fig 18c).
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Figure 10. Medial oblique radiograph depicts early neuropathic changes at the second tarsometatarsal joint in a 34-year-old diabetic man. Intermetatarsal destruction (arrow) is shown.
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Figure 11. Frontal radiograph depicts atrophic neuropathic osteoarthropathy at the tarsometatarsal joints in a 35-year-old diabetic woman. Resorptive changes are present with a Lisfranc pattern of fracture dislocation.
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Figure 12. Frontal radiograph depicts homolateral Lisfranc fracture dislocation in a 60-year-old diabetic woman. Resorption of the middle cuneiform bone (arrow) is shown without associated bone fragments. Fracture dislocation was unsuspected in this patient, who had undergone radiography because she stubbed her toe. (From the ACR Learning File, MSK case 233.)
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Figure 13. Medial oblique radiograph depicts divergent Lisfranc fracture dislocation in a 62-year-old diabetic woman. Second through fifth tarsometatarsal joints are dislocated dorsally and laterally. The navicular cuneiform joint (arrow) is dislocated medially. The patient reported no history of foot trauma.
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Figure 14. Lateral radiograph depicts hypertrophic neuropathic osteoarthropathy of the midfoot in a 63-year-old diabetic woman. Osteophytes (arrow) are larger than those in typical osteoarthritis. This appearance has been referred to as "osteoarthritis with a vengeance" (18).
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Figure 15. Lateral radiograph depicts neuropathic osteoarthropathy of the ankle in a 27-year-old diabetic woman. Large ankle joint effusion with fragmentation and collapse of the tibiotalar joint (solid arrow) is shown. Presence of microvascular calcifications (open arrows) suggests diabetes mellitus as a cause of neuropathic osteoarthropathy. Although less common than neuropathic deformities of the feet, neuropathic ankle changes also occur in patients with diabetic neuropathy.
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Figure 16. Lateral radiograph depicts neuropathic osteoarthropathy of the tibiotalar joint in a 60-year-old diabetic woman. Resorption and fragmentation of the distal tibia and talus (arrow) are shown associated with marked sclerosis, osteophytosis, and periostitis (arrowheads).
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Figure 17. Lateral radiograph depicts neuropathic osteoarthropathy of the ankle and hindfoot in a 42-year-old diabetic man. The distal tibia is resorbed and has sharp margins resembling surgical amputation. The talar dome is resorbed. Sclerosis is present, and subtalar joints (arrows) can no longer be identified.
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Figure 18a. Spontaneous fracture of the fibula and neuropathic osteoarthropathy of the foot in a 63-year-old diabetic woman. (a, b) Anteroposterior (a) and lateral (b) radiographs of the ankle show disruption of the subtalar joint (black arrow in b), talonavicular subluxation, and fracture of the distal fibula (white arrow in a and b). Fractures in ankles of diabetic patients may have limb-threatening consequences. (c) Frontal radiograph depicts collapse of the head of the second metatarsal (arrow). Osseous resorption leads to flattening and fragmentation of metatarsal heads. "Amputations" of the first and fourth toes and vascular calcifications are noted.
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Figure 18b. Spontaneous fracture of the fibula and neuropathic osteoarthropathy of the foot in a 63-year-old diabetic woman. (a, b) Anteroposterior (a) and lateral (b) radiographs of the ankle show disruption of the subtalar joint (black arrow in b), talonavicular subluxation, and fracture of the distal fibula (white arrow in a and b). Fractures in ankles of diabetic patients may have limb-threatening consequences. (c) Frontal radiograph depicts collapse of the head of the second metatarsal (arrow). Osseous resorption leads to flattening and fragmentation of metatarsal heads. "Amputations" of the first and fourth toes and vascular calcifications are noted.
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Figure 18c. Spontaneous fracture of the fibula and neuropathic osteoarthropathy of the foot in a 63-year-old diabetic woman. (a, b) Anteroposterior (a) and lateral (b) radiographs of the ankle show disruption of the subtalar joint (black arrow in b), talonavicular subluxation, and fracture of the distal fibula (white arrow in a and b). Fractures in ankles of diabetic patients may have limb-threatening consequences. (c) Frontal radiograph depicts collapse of the head of the second metatarsal (arrow). Osseous resorption leads to flattening and fragmentation of metatarsal heads. "Amputations" of the first and fourth toes and vascular calcifications are noted.
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Figure 19a. Neuropathic changes in the talonavicular joint in a 27-year-old diabetic woman. (a) Lateral radiograph depicts soft-tissue swelling and effusion (arrow) that overlie early osseous fragmentation of the anterior process of the talus. (b) Lateral radiograph obtained 1 year later shows destruction, sclerosis, and bone fragmentation at this joint. The talonavicular joint is the second most favored site, after the tarsometatarsal joints, of involvement with diabetic neuropathic osteoarthropathy of the foot. (From the ACR Learning File, MSK case 233.)
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Figure 19b. Neuropathic changes in the talonavicular joint in a 27-year-old diabetic woman. (a) Lateral radiograph depicts soft-tissue swelling and effusion (arrow) that overlie early osseous fragmentation of the anterior process of the talus. (b) Lateral radiograph obtained 1 year later shows destruction, sclerosis, and bone fragmentation at this joint. The talonavicular joint is the second most favored site, after the tarsometatarsal joints, of involvement with diabetic neuropathic osteoarthropathy of the foot. (From the ACR Learning File, MSK case 233.)
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Figure 20a. Neuropathic arthropathy in a 65-year-old diabetic man. Axial proton-density-weighted spin-echo (2,500/45) (a) and sagittal inversion-recovery (4,000/60/160 [inversion time msec]) (b) MR images show medial talar dislocation and effusion. Extensive soft-tissue edema is present about the ankle and foot. Soft-tissue edema is commonly seen in neuropathic osteoarthropathy owing to the lack of sympathetic vasoconstriction.
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Figure 20b. Neuropathic arthropathy in a 65-year-old diabetic man. Axial proton-density-weighted spin-echo (2,500/45) (a) and sagittal inversion-recovery (4,000/60/160 [inversion time msec]) (b) MR images show medial talar dislocation and effusion. Extensive soft-tissue edema is present about the ankle and foot. Soft-tissue edema is commonly seen in neuropathic osteoarthropathy owing to the lack of sympathetic vasoconstriction.
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Figure 21. Frontal radiograph depicts neuropathic osteoarthropathy of the forefoot in a 42-year-old diabetic woman. Atrophic changes have resulted in "pointed bones" (white arrows). The first metatarsophalangeal joint has a mortar-in-pestle configuration (black arrow). The radiographic pattern is usually of atrophic neuropathic osteoarthropathy in the forefoot.
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Figure 22. Lateral radiograph depicts neuropathic destruction of the naviculocuneiform joint (arrow) in a 52-year-old diabetic man. Neuropathic osteoarthropathy typically involves the medial column of the foot earlier and more frequently than the lateral column.
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Diabetic neuropathic arthropathy most often affects the foot and ankle, but other locations of osteoarthropathy such as the knees, hips, spine, or wrists may occur. Patients with chronic alcoholism may experience peripheral sensory and motor neuropathy, which also most commonly
affects the lower extremity, especially the forefoot (20–22).
Compared with the ankle and foot, neuropathic involvement of the hip is relatively rare, probably because the hip is subjected to less wear and tear and has a more abundant nerve supply than do more peripheral joints. Neuropathic osteoarthropathy of the hips may present as atrophic or hypertrophic joints (Fig 23) or simply as fractures, usually of the femoral neck (23) (Fig 24).
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Figure 23. Frontal radiograph depicts bilateral neuropathic hips in a 28-year-old man with paraplegia below T7. The right hip is atrophic with an amputated appearance (solid arrow), and the left hip shows hypertrophic sclerosis and fragmentation (open arrow). Bilateral dislocation is shown.
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Figure 24. Frontal radiograph depicts a hip fracture in a 36-year-old woman with alcoholic cirrhosis and a 3-month history of hip pain but no trauma. A high subcapital fracture extends into the femoral neck (arrowheads). This pattern is not typical of traumatic injury or avascular necrosis and is thought to represent neuropathic fracture in an early Charcot hip.
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Neuropathic injuries of the lower extremities can occur in children and most commonly present as epiphyseal separations, but they can also appear as neuropathic osteoarthropathy, metaphyseal fractures, or midshaft fractures of long bones (24). Neuropathic fractures of the lower extremity are common in patients with meningomyeloceles immobilized after spinal fixation surgery (25) (Fig 25). In the pediatric population, differential considerations for neuropathic osteoarthropathy in the lower extremity include congenital indifference or insensitivity to pain (Figs 26, 27) and hereditary sensory and motor peripheral nerve neuropathies (25).
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Figure 25. Frontal radiograph depicts spontaneous fracture in a 10-year-old girl with a meningomyelocele. Femoral location, transverse orientation (black arrows), and exuberant callus (white arrows) due to continued activity are typically seen in fractures of neuropathic origin.
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Figure 26a. Frontal radiographs depict results of congenital indifference to pain in a 17-year-old boy. (a) Left knee is dislocated and deformed. Old stress fracture (arrow) is present along the left medial tibial shaft. (b) Severe atrophic neuropathic changes are shown in the right ankle with disappearance of the talus and mechanical erosion of the calcaneus bone. Note the amputated appearance of the tibia and fibula distally (arrows). (From the ACR Learning File, MSK case 236.)
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Figure 26b. Frontal radiographs depict results of congenital indifference to pain in a 17-year-old boy. (a) Left knee is dislocated and deformed. Old stress fracture (arrow) is present along the left medial tibial shaft. (b) Severe atrophic neuropathic changes are shown in the right ankle with disappearance of the talus and mechanical erosion of the calcaneus bone. Note the amputated appearance of the tibia and fibula distally (arrows). (From the ACR Learning File, MSK case 236.)
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Figure 27a. Congenital insensitivity to pain in a 17-year-old boy. (a) Frontal radiograph of the knee shows destruction and fragmentation of the femoral condyle (arrow). (b) Sagittal T2-weighted spin-echo MR image (2,500/80) shows an osteochondral loose body (arrow) floating in an enormous joint effusion.
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Figure 27b. Congenital insensitivity to pain in a 17-year-old boy. (a) Frontal radiograph of the knee shows destruction and fragmentation of the femoral condyle (arrow). (b) Sagittal T2-weighted spin-echo MR image (2,500/80) shows an osteochondral loose body (arrow) floating in an enormous joint effusion.
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Summary
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Neuropathic osteoarthropathy is the common end result of a wide variety of diseases that share the occurrence of neurosensory loss as the pathophysiologic cause. Anatomic location of the osseous and joint findings, age of the patient, and clinical history may provide clues to the underlying disease responsible for the sensory deficit. Radiologic findings may, at times, be confused with those of osteoarthritis, tumor, and infection. Diabetes mellitus is currently the most common cause of neuropathic osteoarthropathy and most frequently affects the foot. Involvement of the non–weight-bearing joints of the upper extremity is less common and is most often due to syringomyelia. Neuropathic osteoarthropathy of the spine may appear similar to vertebral osteomyelitis and is often a diagnosis of exclusion after disk aspiration, even in patients with conditions predisposing to neuropathic disease. However, the imaging findings of neuropathic osteoarthropathy of the spine can be diagnostic if recognized appropriately. It is important that radiologists are familiar with the various appearances of neuropathic osteoarthropathy since the radiologic findings may be the first clue to the proper diagnosis.
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Footnotes
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2 Current address: 1306 Marina Bay Dr 106-C, Clear Lake Shores, TX 77565. 
3 Current address: Department of Radiology, University of Colorado Health Sciences Center, Denver.
Abbreviation: ACR = American College of Radiology
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References
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Abstract
LEARNING OBJECTIVES 
