Medically reviewed by Dr. Tom Biernacki, DPM — Board-Certified Podiatric Surgeon — Balance Foot & Ankle, Howell & Bloomfield Hills, MI. Last updated April 2026.

Medically Reviewed by Dr. Thomas Biernacki, DPM · Board-Certified Podiatrist · Balance Foot & Ankle Specialists · Last updated April 2026

Table of Contents

• What Is Charcot Foot?
• Causes and Risk Factors
• How Charcot Foot Develops: The Inflammatory Cascade
• Charcot Foot Classification Systems
• Signs and Symptoms by Stage
• Diagnosis and Advanced Imaging
• Conservative Treatment: Offloading and Immobilization
• Surgical Reconstruction for Charcot Deformity
• Essential Foot Care Products for Charcot Patients
• Complete Charcot Foot Protection Kit
• Most Common Mistake
• Warning Signs
• Watch: Charcot Foot Explained
• Frequently Asked Questions
• Sources
• Schedule Your Evaluation

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What Is Charcot Foot? Understanding This Limb-Threatening Condition

Charcot foot — formally known as Charcot neuroarthropathy (CN) or neuropathic osteoarthropathy — is a progressive, destructive condition affecting the bones, joints, and soft tissues of the foot and ankle that occurs in individuals with significant peripheral neuropathy. First described by Jean-Martin Charcot in 1868 in patients with tabes dorsalis (neurosyphilis), the condition is now overwhelmingly associated with diabetes mellitus, which accounts for more than 90% of Charcot foot cases seen in modern clinical practice.

The fundamental mechanism underlying Charcot foot is the loss of protective sensation combined with continued weight-bearing. When the foot cannot detect pain from repetitive microtrauma, stress fractures, or joint subluxation, the normal protective responses (limping, offloading, seeking medical attention) do not occur. The patient continues walking on a progressively damaged skeleton, creating a catastrophic cycle of fragmentation, fracture, dislocation, and deformity that can transform a normally aligned foot into a shapeless mass of disorganized bone in a matter of weeks to months.

The scope of this condition is staggering. Charcot foot affects an estimated 0.1-7.5% of the diabetic population, with higher rates in patients with existing neuropathy and prior foot ulceration. The condition carries a significant risk of major lower extremity amputation — studies report amputation rates of 15-25% in patients with established Charcot deformity, primarily due to recurrent ulceration, deep infection, and osteomyelitis that develop beneath the deformed bony architecture. Early diagnosis and aggressive management are the keys to limb preservation.

Causes and Risk Factors for Charcot Neuroarthropathy

While diabetes mellitus is the dominant etiology in contemporary practice, Charcot neuroarthropathy can develop in any condition that produces significant peripheral neuropathy. Understanding the full spectrum of causative conditions helps clinicians maintain appropriate vigilance in high-risk populations and avoid the diagnostic tunnel vision that can delay recognition in non-diabetic patients.

Diabetes mellitus is the cause in more than 90% of Charcot foot cases. The risk increases dramatically with duration of diabetes, degree of glycemic control, and severity of neuropathy. Patients with diabetes for more than 10 years, HbA1c consistently above 8%, and dense peripheral neuropathy (loss of protective sensation on monofilament testing) are at highest risk. Additional risk factors include obesity, renal disease requiring dialysis, prior foot ulceration, and history of minor foot trauma.

Other neuropathic conditions that can cause Charcot foot include chronic alcoholism (the second most common cause), spinal cord injury, peripheral nerve injury, HIV/AIDS neuropathy, Charcot-Marie-Tooth disease, and syringomyelia. Rare but documented causes include leprosy, heavy metal toxicity, and drug-induced neuropathy from chemotherapy agents such as vincristine and cisplatin. In Michigan, where we see a substantial population of patients with diabetic neuropathy and alcohol-related neuropathy, maintaining awareness of both etiologies is essential for early detection.

The triggering event for acute Charcot is often identifiable in retrospect — a minor sprain, a stumble on uneven ground, recent foot surgery, or even just a change in activity level. Because the patient cannot feel the injury, the inflammatory response proceeds unchecked while the patient continues to bear weight on the damaged structures. In our Southeast Michigan practice, we commonly see Charcot episodes triggered by unnoticed injuries during winter walks on icy sidewalks, yard work during the spring season, and barefoot walking on hot summer pavement.

How Charcot Foot Develops: The Inflammatory Cascade

The pathophysiology of Charcot foot has been debated for over a century, with two competing theories — the neurotraumatic theory and the neurovascular theory — eventually merging into a unified model that explains the condition’s complex pathogenesis. Understanding this mechanism is essential for appreciating why early intervention is so critical and why continued weight-bearing during the acute phase is so destructive.

The neurotraumatic theory proposes that loss of protective sensation allows repetitive mechanical trauma and unrecognized fractures to accumulate without the normal pain-mediated protective responses. The patient continues ambulating on a progressively damaged foot, creating a cycle of fracture, attempted healing, and re-fracture that overwhelms the bone’s ability to repair itself. This theory explains the strong association between Charcot foot and dense peripheral neuropathy, as well as the frequent identification of triggering traumatic events.

The neurovascular theory proposes that autonomic neuropathy causes loss of sympathetic vascular tone, resulting in increased blood flow to the foot and enhanced osteoclastic bone resorption. This hyperemic state weakens bone at the structural level, making it susceptible to fracture under normal weight-bearing loads. The neurovascular theory explains the characteristic warmth, erythema, and bounding pulses observed in acute Charcot foot, as well as the osteopenia that frequently precedes clinical fragmentation.

The current unified RANKL/OPG inflammatory model integrates both theories and adds a critical molecular mechanism. Following initial trauma (neurotraumatic trigger) in the setting of increased blood flow (neurovascular component), an unregulated inflammatory cascade develops. Proinflammatory cytokines — particularly TNF-α, IL-1β, and IL-6 — upregulate the RANK ligand (RANKL) pathway, which stimulates massive osteoclast differentiation and activation. Simultaneously, the protective osteoprotegerin (OPG) pathway that normally counterbalances osteoclastic activity is suppressed. The result is rapid, aggressive bone resorption that produces the dramatic fragmentation and dissolution characteristic of acute Charcot foot. This molecular understanding has opened potential therapeutic avenues, including bisphosphonate therapy and anti-RANKL agents.

Charcot Foot Classification Systems

Two classification systems are widely used in clinical practice to describe and stage Charcot foot. The Eichenholtz classification describes the temporal progression of the disease, while the Sanders and Frykberg anatomic classification identifies the specific joints and regions affected. Together, these systems guide treatment decisions and help predict outcomes.

The Eichenholtz classification divides Charcot into three stages. Stage 0 (Prodromal), added later to the original classification, describes the pre-radiographic phase where clinical signs of inflammation are present (warmth, swelling, erythema) but standard radiographs appear normal or show only subtle osteopenia. MRI during this stage reveals bone marrow edema and soft tissue inflammation — this is the critical window for intervention where prompt offloading can prevent progression to destructive changes. Stage I (Development/Fragmentation) demonstrates active bone destruction with periarticular fractures, joint subluxation or dislocation, and bony debris on radiographs. The foot is hot, severely swollen, and clinically indistinguishable from infection without advanced imaging. Stage II (Coalescence) shows evidence of healing with absorption of bone debris, sclerosis of fracture fragments, and early fusion of affected joints. Clinically, the warmth and swelling begin to subside. Stage III (Reconstruction/Consolidation) represents the healed but deformed state, with mature bony fusion, remodeling of fracture fragments, and residual architectural deformity that requires long-term accommodative management.

The Sanders and Frykberg anatomic classification identifies five patterns based on the joints involved. Pattern I (15% of cases) affects the forefoot at the metatarsophalangeal and interphalangeal joints. Pattern II (40% of cases) affects the tarsometatarsal (Lisfranc) joints — this is the most common pattern and frequently produces the classic rocker-bottom deformity. Pattern III (30% of cases) involves the midtarsal joints (talonavicular, calcaneocuboid). Pattern IV (10% of cases) affects the ankle joint. Pattern V (5% of cases) involves the calcaneus. Patterns IV and V carry the worst prognosis due to the difficulty of achieving stable reconstruction and the high rates of amputation.

Signs and Symptoms of Charcot Foot by Stage

The clinical presentation of Charcot foot varies dramatically depending on the stage of the disease. The challenge — and the reason for frequent diagnostic delays — is that the acute presentation mimics several common conditions including cellulitis, deep vein thrombosis, gout, and septic arthritis. The average delay from symptom onset to correct diagnosis is still an alarming 29 weeks in published literature, a statistic that directly contributes to the severity of deformity that develops before treatment is initiated.

Acute Charcot (Stage 0-I): The hallmark presentation is a unilateral hot, red, swollen foot in a patient with peripheral neuropathy. The affected foot is typically 2-6°C warmer than the contralateral foot on infrared thermometry. Swelling is often dramatic, extending from the toes to the ankle. The skin appears erythematous and shiny. Despite these alarming inflammatory signs, the patient reports relatively little pain — a critical diagnostic clue that should immediately raise suspicion for Charcot in any neuropathic patient. Some patients note a vague aching or “fullness” in the foot, but the dramatic disconnect between the severity of the clinical appearance and the minimal pain reported is pathognomonic. Joint instability, crepitus, and abnormal motion may be palpable in Stage I as bony architecture fails.

Chronic Charcot (Stage II-III): As the acute inflammatory phase resolves, the foot assumes its final deformed configuration. The classic rocker-bottom deformity develops when Pattern II or III Charcot collapses the midfoot arch, creating a convex plantar surface with a bony prominence at the apex of the collapse. This prominence is the most dangerous feature of Charcot deformity because it creates a focal point of extreme pressure concentration during weight-bearing that inevitably leads to callus formation, ulceration, and deep infection if not adequately accommodated with custom orthotic devices and therapeutic footwear. Other deformities include medial or lateral midfoot subluxation, ankle valgus (from Pattern IV Charcot), and forefoot adduction or abduction.

Diagnosis and Advanced Imaging for Charcot Foot

Diagnosing Charcot foot requires a high index of clinical suspicion combined with appropriate imaging. The clinical dictum that every podiatrist should carry is simple: any unilateral hot, swollen foot in a diabetic patient is Charcot foot until proven otherwise. This presumptive approach, while potentially leading to some overdiagnosis, dramatically reduces the catastrophic delays that allow preventable deformity to develop.

Clinical assessment begins with bilateral comparison of skin temperature using an infrared dermal thermometer. A temperature difference of more than 2°C between the affected and contralateral foot is highly suggestive of acute Charcot in the appropriate clinical context. The “elevation test” provides additional diagnostic information — in Charcot foot, swelling typically reduces significantly with 5-10 minutes of elevation, while swelling from deep infection tends to persist. Vascular assessment with palpation of pedal pulses and ankle-brachial index measurement is essential because Charcot foot requires adequate blood supply for the healing process, and concurrent peripheral arterial disease significantly complicates management.

Weight-bearing radiographs remain the first-line imaging study, though they are frequently normal or show only subtle osteopenia in Stage 0 Charcot. Standard views include AP, lateral, and oblique projections of the foot, plus AP and lateral ankle views when ankle involvement is suspected. Characteristic radiographic findings in Stage I include periarticular fractures, joint subluxation or dislocation, bony fragmentation, and subchondral bone resorption. The lateral view is particularly valuable for assessing midfoot collapse — loss of the normal talar-first metatarsal angle (Meary’s angle) indicates tarsometatarsal or midtarsal subluxation.

MRI is the most valuable advanced imaging study for Charcot foot, particularly in Stage 0 when radiographs are negative. MRI reveals bone marrow edema, soft tissue inflammation, occult fractures, and ligamentous disruption that precede radiographically visible changes by weeks to months. The critical challenge with MRI is distinguishing acute Charcot from osteomyelitis, as both conditions produce bone marrow edema and soft tissue changes. Features favoring Charcot include preservation of the subchondral plate, periarticular distribution of marrow edema, joint effusion without cortical destruction, and absence of a skin ulcer or sinus tract overlying the affected area. Features favoring osteomyelitis include cortical destruction with geographic marrow replacement, adjacent soft tissue abscess, and a contiguous skin ulcer with direct communication to bone.

Nuclear medicine studies including bone scintigraphy (technetium-99m bone scan) and labeled white blood cell scanning can help differentiate Charcot from infection when MRI findings are equivocal. The combination of a positive bone scan with a negative or only mildly positive white blood cell scan supports a diagnosis of acute Charcot without superimposed infection. PET-CT with fluorodeoxyglucose (FDG) has also shown promise in this differential diagnosis, though its availability and cost limit widespread use.

Conservative Treatment: Offloading and Immobilization

The cornerstone of acute Charcot foot treatment is immediate, complete, non-negotiable offloading. The single most important intervention in Charcot management is removing all mechanical stress from the affected foot before further bony destruction occurs. Every day of continued unprotected weight-bearing during the acute phase contributes to additional fractures, progressive joint destruction, and worsening deformity that may ultimately require complex surgical reconstruction or amputation to manage.

Total contact casting (TCC) is the gold standard for acute Charcot foot immobilization and offloading. The TCC distributes weight-bearing forces evenly across the entire plantar surface and lower leg, eliminates shear forces, reduces edema through circumferential compression, and prevents the patient from removing the device (compliance being a significant challenge in neuropathic patients who cannot feel the consequences of non-compliance). Casts are changed every 1-2 weeks initially as swelling subsides, then every 2-4 weeks as the foot stabilizes. The total duration of casting typically ranges from 3-6 months for Pattern I-III Charcot, with progression from TCC to a removable cast walker or Charcot restraint orthotic walker (CROW boot) once temperature differential between feet normalizes to less than 2°C.

The CROW boot (Charcot Restraint Orthotic Walker) is a custom-fabricated, total-contact, bivalved ankle-foot orthosis that provides long-term protection for the consolidated Charcot foot. The CROW is typically used as a transitional device between casting and definitive therapeutic footwear, though some patients with severe residual deformity require lifelong CROW use. The device is fabricated from rigid thermoplastic lined with accommodative foam, custom-molded to the patient’s foot and ankle to distribute pressure evenly and protect bony prominences.

Therapeutic footwear and custom orthotic insoles are the long-term management solution for patients with consolidated Charcot deformity. Extra-depth or custom-molded shoes with rigid rocker-bottom soles reduce midfoot bending stress, while custom-molded total contact insoles redistribute plantar pressure away from bony prominences. PowerStep Orthotic Insoles serve as an excellent foundation for patients transitioning from CROW boots to therapeutic footwear, providing structured arch support and deep heel cupping that maintain hindfoot alignment and reduce midfoot stress concentration. For patients whose deformity is mild enough to accommodate in standard footwear, PowerStep insoles provide an immediately available, clinically appropriate interim solution while custom devices are being fabricated.

Surgical Reconstruction for Charcot Foot Deformity

Surgical intervention for Charcot foot is indicated when conservative management cannot achieve a stable, plantigrade, braceable foot — or when recurrent ulceration and infection threaten the viability of the limb. The decision to operate on a Charcot foot is among the most consequential in foot and ankle surgery, requiring careful consideration of the patient’s vascular status, nutritional state, glycemic control, bone quality, infection status, and ability to comply with the demanding postoperative protocol. Surgery during the acute inflammatory phase (Eichenholtz Stage I) is generally contraindicated unless emergent debridement or stabilization is required.

Exostectomy (bony prominence removal) is the simplest surgical option for Charcot deformity and is indicated when a focal plantar bony prominence creates recurrent ulceration that cannot be managed with custom orthotic accommodation alone. The procedure involves removal of the offending bony prominence through a midfoot approach, followed by primary closure and prolonged offloading. While exostectomy addresses the immediate ulceration risk, it does not correct the underlying deformity and may alter the biomechanical environment in ways that create new pressure points elsewhere. Success rates for ulcer healing after exostectomy are approximately 75-85% at one year.

Midfoot arthrodesis with internal fixation is the current standard for reconstruction of unstable or severely deformed Charcot midfoot (Pattern II-III). The procedure involves realignment of the midfoot to a plantigrade position, debridement of nonviable bone and cartilage, and rigid internal fixation to maintain correction until bony fusion is achieved. Modern fixation techniques include plantar locking plates (which resist the deforming dorsal subluxation forces), intramedullary beams (large bolts that span the entire midfoot from calcaneus to metatarsals), and supplementary external fixation. The goal is to create a stable, plantigrade foot that can be accommodated in therapeutic footwear and custom orthotics without recurrent ulceration.

Ankle and hindfoot reconstruction for Pattern IV-V Charcot is the most challenging procedure in Charcot surgery. Tibiotalocalcaneal (TTC) arthrodesis using retrograde intramedullary nailing is the workhorse procedure for Charcot ankle and subtalar destruction. The nail provides mechanical stability across the entire hindfoot while fusion progresses — a process that frequently requires 4-6 months or longer in the compromised metabolic environment of Charcot bone. Supplementary fixation with screws, plates, or circular external fixation (Ilizarov frame) may be necessary for severely osteopenic bone or when infection requires staged reconstruction. Despite advances in technique and fixation, the nonunion rate for Charcot TTC arthrodesis remains 10-30%, and the amputation rate following failed reconstruction approaches 50%.

Postoperative management after Charcot reconstruction is prolonged and demanding. Patients typically remain non-weight-bearing for 8-12 weeks minimum, followed by protected weight-bearing in a walking boot or TCC for an additional 4-8 weeks. Total protected weight-bearing duration frequently exceeds 6 months. Nutritional optimization, glycemic control (target HbA1c below 8% and ideally below 7%), smoking cessation, and vitamin D supplementation are critical adjuncts that significantly influence healing rates and outcomes.

Essential Foot Care Products for Charcot Patients

Managing Charcot foot requires a comprehensive approach that extends beyond clinical visits. The right foot care products can significantly reduce the risk of ulceration, manage chronic swelling, and provide the daily protection that Charcot patients need to maintain their mobility and limb integrity. At Balance Foot & Ankle, we recommend a three-product protocol that addresses the critical daily management needs for patients in the post-acute and chronic phases of Charcot foot.

PowerStep Orthotic Insoles provide the biomechanical foundation for daily foot protection in Charcot patients with mild-to-moderate deformity. The structured arch support prevents further midfoot collapse during weight-bearing, while the deep heel cup maintains calcaneal alignment and reduces lateral ankle instability that frequently accompanies hindfoot Charcot. For patients transitioning from CROW boots to therapeutic footwear, PowerStep insoles offer an immediately available, clinically appropriate solution that provides substantially more support than the flat insoles found in standard shoes. While patients with severe deformity require custom-molded total contact insoles, PowerStep serves as an excellent bridge device and ongoing solution for patients whose deformity has been surgically corrected to a near-normal alignment.

Doctor Hoy’s Natural Pain Relief Gel addresses the paradox of Charcot foot pain management. While the underlying neuropathy reduces protective sensation, many Charcot patients experience deep aching, burning neuropathic pain, and inflammatory discomfort that is distinct from the absent superficial sensation. Doctor Hoy’s natural arnica and menthol formula provides topical analgesia that can be applied directly to the affected area without the systemic side effects of oral medications — a particularly important consideration in diabetic patients who frequently take multiple medications for glycemic control, hypertension, and cardiovascular risk reduction. The topical application also provides a therapeutic ritual that encourages daily foot inspection, which is one of the most important preventive behaviors for diabetic foot care.

DASS Medical Grade Compression Socks address the chronic edema that persists in many Charcot patients long after the acute phase has resolved. Graduated compression supports venous return, reduces dependent swelling that contributes to skin breakdown, and provides proprioceptive feedback that helps compensate for the lost protective sensation. For Charcot patients, consistent use of medical-grade compression can mean the difference between skin that remains intact and skin that breaks down under the combined stress of pressure, moisture, and edema. We recommend wearing DASS compression socks during all upright hours, removing them only for bathing and sleep.

Complete Charcot Foot Protection Kit

Most Common Mistake: Dismissing the Hot, Swollen Foot as Infection

Warning Signs: When to Seek Emergency Charcot Foot Evaluation

Watch: Charcot Foot Explained

https://www.youtube.com/watch?v=A11FFjCXAX4

Frequently Asked Questions About Charcot Foot

What causes Charcot foot and who is most at risk?

Charcot foot is caused by a combination of peripheral neuropathy (loss of protective sensation) and continued weight-bearing on a damaged foot skeleton. Diabetes mellitus accounts for more than 90% of cases. The highest-risk patients are those with diabetes for more than 10 years, dense peripheral neuropathy confirmed on monofilament testing, poor glycemic control (HbA1c above 8%), prior foot ulceration, obesity, and renal disease. The triggering event is often minor trauma — a stumble, a minor sprain, or recent foot surgery — that goes unrecognized due to absent pain sensation.

How can I tell the difference between Charcot foot and a foot infection?

Both conditions can present with a hot, red, swollen foot, making differentiation challenging. Key differences: Charcot foot typically occurs without an obvious wound or portal of entry, the patient reports minimal pain despite severe-appearing inflammation, and the swelling improves significantly with elevation. Infection usually has an identifiable wound, may produce purulent drainage or systemic signs (fever, elevated white blood cell count), and the swelling persists despite elevation. However, Charcot and infection can coexist, which is why advanced imaging with MRI and laboratory studies are often necessary for definitive diagnosis.

Can Charcot foot be cured or reversed?

Charcot foot cannot be reversed once bony destruction has occurred, but it can be effectively managed to prevent further deformity and preserve the limb. If caught in Stage 0 (before radiographic changes), prompt immobilization and offloading can prevent permanent deformity entirely. Once deformity develops (Stages I-III), the goals shift to achieving a stable, plantigrade foot through casting and potentially surgical reconstruction, then maintaining it with therapeutic footwear and custom orthotics. With comprehensive management, the vast majority of Charcot feet can be preserved — amputation is a last resort, not an inevitability.

How long does Charcot foot treatment take?

Active treatment for acute Charcot foot typically requires 3-6 months of immobilization in total contact casts, followed by 3-6 months of transitional bracing in a CROW boot or removable cast walker. Patients who require surgical reconstruction face 6-12 months of protected weight-bearing during the healing period. After the acute phase resolves, Charcot foot requires lifelong management with therapeutic footwear, custom orthotics, regular podiatric monitoring, and daily self-inspection. Temperature monitoring of both feet (comparing side to side) should become a permanent daily routine.

Is surgery always necessary for Charcot foot?

No — many Charcot feet can be successfully managed without surgery. Conservative treatment with total contact casting, transitional bracing, and long-term therapeutic footwear is appropriate and effective for patients whose feet consolidate in a reasonably plantigrade alignment that can be accommodated with custom orthotics. Surgery is reserved for specific indications: recurrent ulceration despite optimal conservative management, unstable deformity that cannot be braced, severe malalignment creating unmanageable pressure points, or infected bone requiring debridement. The decision to operate is highly individualized based on deformity pattern, location, bone quality, vascular status, and the patient’s overall health.

Sources

1. Rogers LC, et al. “The Charcot foot in diabetes.” Diabetes Care. 2011;34(9):2123-2129.
2. Rosenbaum AJ, DiPreta JA. “Classifications in brief: Eichenholtz classification of Charcot arthropathy.” Clinical Orthopaedics and Related Research. 2015;473(3):1168-1171.
3. Wukich DK, Sung W. “Charcot arthropathy of the foot and ankle: modern concepts and management review.” Journal of Diabetes and Its Complications. 2009;23(6):409-426.
4. Pinzur MS, et al. “Current practice patterns in the treatment of Charcot foot.” Foot & Ankle International. 2016;37(12):1335-1339.
5. Jeffcoate WJ, et al. “The role of proinflammatory cytokines in the cause of neuropathic osteoarthropathy (acute Charcot foot) in diabetes.” The Lancet. 2005;366(9502):2058-2061.

Schedule Your Charcot Foot Evaluation at Balance Foot & Ankle

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Charcot Foot Treatment at Balance Foot & Ankle

Charcot foot is a serious complication of peripheral neuropathy that can lead to permanent deformity if not treated promptly. Our podiatric surgeons have extensive experience managing Charcot neuroarthropathy at our Howell and Bloomfield Hills offices.

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Clinical References

1. Rogers LC, et al. The Charcot foot in diabetes. Diabetes Care. 2011;34(9):2123-2129. doi:10.2337/dc11-0844
2. Lowery NJ, et al. Surgical management of Charcot neuroarthropathy of the foot and ankle: a systematic review. Foot Ankle Int. 2012;33(2):113-121. doi:10.3113/FAI.2012.0113
3. Frykberg RG, Belczyk R. Epidemiology of the Charcot foot. Clin Podiatr Med Surg. 2008;25(1):17-28. doi:10.1016/j.cpm.2007.10.001