Tag Archives: diabetic neuropathy

Overview of diabetic neuropathy and review of FDA-approved oral therapies

by Ebony Love DPM DABPM1*, Michelle Garcia MS2, Ziad Labbad MD DPM CPed3

The Foot and Ankle Online Journal 13 (4): 2

Diabetic neuropathy is the most common complication of uncontrolled and chronic diabetes. Neuropathy is the result when the somatosensory system is compromised leaving patients with irreversible nerve damage. The continuity of this neuropathic pain may lead to disorders such as insomnia, depression, and anxiety. The cause of neuropathic pain cannot be treated, and current treatment management focuses on treating the symptoms. A review of current literature on diabetic neuropathy and of FDA approved oral therapies is performed to provide an extensive overview in order to reduce and prevent the progression of this disease. The epidemiology of diabetic neuropathy can be characterized by its prevalence and risk factors. Symmetric polyneuropathy is the most common type of diabetic neuropathy accounting for about 75% of affected patients and is divided into classes depending on the types of sensory fibers involved. Small fiber neuropathy is associated with burning, prickling pain due to non-painful stimuli or an exaggerated response to painful stimuli. Large fiber affected neuropathy involves numbness, tingling without pain, and loss of protective sensation. Besides lifestyle intervention and glucose control the first line medication for diabetic neuropathy is gabapentin, pregabalin and duloxetine. This literature review guide is dedicated to the millions suffering from diabetic neuropathy. Neuropathic pain is a chronic disorder that can impair a patient’s quality of life. The results of this literature review demonstrate a need for long-term research with advancing technologies on new medications to understand their specific effects and risks to patients.

Keywords: diabetic neuropathy, gabapentin, duloxetine, cymbalta, FDA warning for gabapentinoids

ISSN 1941-6806
doi: 10.3827/faoj.2020.1304.0002

1 – Clinical Associate Professor Temple University School of Podiatric Medicine, Medicine Department , Philadelphia, PA.
2 – Podiatric Student Temple University School of Podiatric Medicine
3 – Clinical Professor Temple University School of Podiatric Medicine, Biomechanics and Medicine Department
* – Corresponding author: elove@temple.edu

Diabetic neuropathy is the most common complication of uncontrolled and chronic diabetes. Neuropathy is the result of a compromised somatosensory system leaving patients with irreversible nerve damage [1,2]. The progression of this neuropathic pain may lead to disorders such as insomnia, depression, anxiety, and impaired quality of life [1,2]. This common complication of diabetes is correlated to increase doctor visits and increase prescription of medication [2]. Currently, treatment management for diabetic neuropathic pain focuses on treating the symptoms due to the irreversible nerve damage [1,2].

Our goal was to provide an overview of diabetic neuropathy and oral treatment options including a recent update of the new FDA warnings on gabapentinoids.


Thorough research of literature via PubMed concerning (i) the etiology of diabetic neuropathy; (ii) symptom presentation (iii) FDA approved oral medications for patients with neuropathic pain was reviewed.


Epidemiology of Diabetic Neuropathy

The epidemiology of diabetic neuropathy can be characterized by its prevalence and risk factors such as lifestyle, comorbidities, and genetics. The prevalence of diabetes mellitus is 419 million adults worldwide (8.8% of the adult population), in which 50% of affected individuals will progress to develop polyneuropathy [3]. There is a high correlation of diabetic neuropathy in patients with obesity and increased waist circumference [3]. Clinical setting risks of diabetic neuropathy include comorbidities such as a high HbA1c, duration of diabetes disease, and poor glucose control [3]. For heredity causes, the opioid receptor gene (OPRM1) and sodium channel gene (SCN9A) showed significant association with diabetic neuropathy; it has been reported in one study that 56% of participants has reported a family member with diabetic neuropathy [3].

Signs and Symptoms of Diabetic Neuropathy

There are different types of diabetic neuropathy: symmetric polyneuropathy, autonomic neuropathy, and cardiovascular autonomic neuropathy [1,2]. Symmetric polyneuropathy is the most common type of diabetic neuropathy accounting for about 75% of affected patients [1]. The distribution of diabetic polyneuropathy includes a “stocking and glove” pattern because neuropathy typically affects the longest nerves of the body the most hence the feet, legs, hands, and forearms are the sites of the majority of symptoms [2]. Diabetic polyneuropathy is further divided into classes depending on the types of sensory fibers involved [1,2]. Small fiber neuropathy is associated with burning, prickling pain due to non-painful stimuli or an exaggerated response to painful stimuli. Clinical tests for small-fiber function include pinprick and temperature sensations [1]. Large fiber affected neuropathy involves numbness, tingling without pain, and loss of protective sensation. Due to the loss of protective sensations, large fiber affected neuropathy is associated as a high risk factor for foot ulcerations and amputations [1]. Clinical tests for large-fiber function include vibration perception with 128-Hz, proprioception, 10-g monofilament and ankle reflexes. Patients should be assessed for distal polyneuropathy starting at diagnosis of type 2 diabetes or five years after the diagnosis of type 1 diabetes with at least annual exams thereafter [1,2,3,4]. It is important to note that up to 50% of patients with diabetic neuropathy is asymptomatic which can put these individuals at greater risk for injuries to their feet that lack sensation [1]. Prevention and early detection is an important medical practice for diabetic care due to not being able to restore underlying nerve damage.

FDA Approved Oral Medications for Neuropathy Pain

Diabetic neuropathy is hard to treat due to the underlying irreversible nerve damage. At this time there is no medication capable of restoring the nerve damage caused by neuropathy. Current methods of treatment focus on treating the symptoms of diabetic neuropathy supporting “unconventional analgesics” medications including antiepileptics, Gabapentin and Pregabalin, and antidepressant, Duloxetine [1,4,5,6]. It is important to note that the amount of patients who actually receive worthwhile pain relief from any oral listed medication, greater than 50% of pain relief, only occur in about 10% to 25% of the affecting population [4].

Gabapentin acts to bind to α2-δ calcium channels in the central and peripheral nervous system to reduce excitability of nerve cells [4]. Evidence shows patient’s who experience relief of symptoms report at least 50% reduction in pain [1,4]. It is important to note that effective oral dose is at least 1200 mg and noted high correlation with reported successful dosing as high as 3600 mg per day [1,4]. Due to the necessary high doses for the drugs effectiveness to alleviate neuropathic pain there has been numerous reported withdrawal and side effects noted in Gabapentin than other approved oral medications for neuropathic pain [4]. Common side effects seen in patients taking Gabapentin include dizziness, drowsiness, gait disturbances, and hypoventilation; the incidence rates of patients taking this medication who experience these negative side effects ranges 1.1% to 19% of the time [4,8].

Pregabalin also binds to α2-δ calcium channels inhibitory to reduce excitability of nerve cells [6]. Evidence suggests that patients who experience relief of symptoms report 30%-50% improvement in pain [1,6]. The effective dose of Pregabalin is 300 mg or 600 mg per day orally [1,6]. The benefits of Pregabalin include faster onset of action and less necessary dose for effectiveness when compared to Gabapentin [1]. Similar to Gabapentin reported side effects include dizziness, drowsiness, and gait disturbances; specific side effects to Pregabalin include edema and weight gain [1,6].

Antidepressant Duloxetine binds to norepinephrine and selective serotonin reuptake inhibitors that influence the pain pathway [1,5,6]. Evidence supports the efficacy of Duloxetine for relieving neuropathic pain when compared to Pregabalin and Gabapentin [6]. Effective dose 60 mg and 120 mg everyday orally [1,5,6]. Side effects of Duloxetine include increased blood pressure and lower leg edema [6].

New FDA Warning on Gabapentinoids

Common side effects of gabapentinoids already noted publically is drowsiness and dizziness. However, with the current opioid epidemic there has been a growing concern regarding the overprescribing gabapentinoids for neuropathic pain relief [7]. Additionally, there has been evidence of drug abuse and withdrawal symptoms noted with chronic use [7,8]. Most recently, there has been a new FDA warning label on gabapentinoids due to case reports of respiratory distress in patients with respiratory issues, like COPD, combined with other opioid pain relievers, and combined with other central nervous depressants [9]. Medical professionals should reassess their reliance on first line use of gabapentinoids for treatment of neuropathic pain in patients with respiratory issues.


Neuropathic pain is a chronic disorder that can impair a patient’s quality of life. Management of that pain should be addressed empathetically with a rational approach to manage the pain of neuropathy. The results of this literature review demonstrate a need for further research of the existing neuropathic pain medications to understand their specific effects and risks to patients. In closing, we should also continue to emphasize prevention of the progression of diabetic neuropathy with glucose control and lifestyle modifications.


The authors sincerely acknowledge the Temple University School of Podiatric Medicine, the Medicine Department, for their support.


  1. Pop-Busui R, Boulton AJM, Feldman EL, et al. Diabetic neuropathy: a position statement by the american diabetes association. Dia Care. 2017;40(1):136-154.
  2. Colloca L, Ludman T, Bouhassira D, et al. Neuropathic pain. Nat Rev Dis Primers. 2017;3(1):17002.
  3. Hébert HL, Veluchamy A, Torrance N, Smith BH. Risk factors for neuropathic pain in diabetes mellitus: PAIN. 2017;158(4):560-568.
  4. Wiffen PJ, Derry S, Bell RF, Rice ASC, Tölle TR, Phillips T, Moore RA. Gabapentin for chronic neuropathic pain in adults. Cochrane Database of Systematic Reviews 2017, Issue 6. Art. No.: CD007938..
  5. Raskin J, Pritchett YL, Wang F, et al. A double-blind, randomized multicenter trial comparing duloxetine with placebo in the management of diabetic peripheral neuropathic pain. Pain Med. 2005;6(5):346-356.
  6. Quilici S, Chancellor J, Löthgren M, et al. Meta-analysis of duloxetine vs. pregabalin and gabapentin in the treatment of diabetic peripheral neuropathic pain. BMC Neurol. 2009;9(1):6.
  7. Goodman CW, Brett AS. Gabapentin and pregabalin for pain — is increased prescribing a cause for concern? N Engl J Med. 2017;377(5):411-414.
  8. Quintero GC. Review about gabapentin misuse, interactions, contraindications and side effects. J Exp Pharmacol. 2017;9:13-21.
  9. Research C for DE and. FDA warns about serious breathing problems with seizure and nerve pain medicines gabapentin (Neurontin, gralise, horizant) and pregabalin (Lyrica, lyrica cr). FDA. Published online January 30, 2020. https://www.fda.gov/drugs/drug-safety-and-availability/fda-warns-about-serious-breathing-problems-seizure-and-nerve-pain-medicines-gabapentin-neurontin

Charcot foot management using MASS posture foot orthotics: A case study

by Edward S. Glaser DPM1; David Fleming BS2*; Barbara Glaser2

The Foot and Ankle Online Journal 10 (3): 4

Background: A 62-year old male being treated for Charcot arthropathy of his right foot at the VA Medical Center in Orlando, FL.  The patient was using a knee walker with a below knee cast at onset of treatment.
Methods:  Custom rocker sole walking boot with built in EVA MASS posture orthotic and MASS orthotic Therapy
Results:  Quality of life improvements.  As the Charcot foot remodeled it coalesced into a foot with an increased medial longitudinal arch allowing for return closer to normal gait and footwear.  No ulcerogenesis was noted with aggressive orthotic therapy.  Protective sensation partially returned to feet bilaterally.
Conclusions:  An increase in patient quality of life without introducing ulcers.   More research needs to be done to determine if this treatment protocol contributes to protective sensation returning to patients with DPN.

Keywords: Charcot foot, diabetic neuropathy, orthoses, MASS Posture

ISSN 1941-6806
doi: 10.3827/faoj.2017.1003.0004

1 – Founder and CEO of Sole Supports, Inc.
2 – Sole Supports, Inc.
* – Corresponding author: dfleming@solesupports.com

The patient is a 62-year old, well nourished, caucasian male with a 12-year history of Type II Diabetes Mellitus. He has experienced neuropathy for 9 years and for the last 7 years he has been profoundly numb bilaterally distal to the ankle. Following a 10-month period of misdiagnosis, he was diagnosed with Charcot foot on November 18, 2015, at the Orlando VAMC. Podiatric treatment for four months prior consisted of ambulating in a BK cast with a knee walker. Casts were reapplied every 3-4 weeks. During the four months of immobilization, the patient noted considerable atrophy of the right gastroc-soleus muscle and loss of his medial longitudinal arch. The patient’s right foot had become a semi-rigid rocker sole foot (Figure 1).

Figure 1 Rocker sole foot.

When the patient was first seen, insensitivity was confirmed with a Semmes Weinstein 5.07 monofilament test bilaterally. No ulcers were visibly present. The patient’s right foot had significant swelling and the patient had gone from a size 12.5 USA (M) shoe to a size 14 USA (M) shoe prior to casting according to the patient.

To prevent amputation of his foot, a prospective protocol was created as the patient progressed.  If at any time the patient developed an ulcer, the project would have been terminated and traditional care would have resumed.


A Semmes Weinstein 5.07 monofilament was used to determine the patient’s protective sensation.  The locations for monofilament testing were as follows: the plantar aspect of metatarsal heads and distal phalanges 1,3,5. The plantar aspect of the heel, medial arch, and lateral arch. The dorsal aspect of the skin at the base of metatarsal 3, and plantar aspect of the heel, bilaterally [1].

Figure 2 Paper Test shown with MASS Orthotic.

The Paper Test (Figure 2) consisted of the patient weight bearing on the affected foot with a piece of paper placed under both the forefoot and the rearfoot.  The practitioner then attempted to remove the piece of paper by pulling it anteriorly/posteriorly.  If the paper tore then that was a positive result, if the paper slid out it was a negative result.  A positive result meant that part of the foot was providing adequate force to the ground, resulting in the paper being torn.  A negative result meant that part of the foot was not providing adequate force to the ground and slid out un torn.  The paper test was used to determine when it was appropriate to move him from the custom MASS posture rocker sole shoe boot to the MASS orthotic  inside of a diabetic shoe.

Figure 3  Custom walking boot with EVA Shell MASS Posture Orthotic.

Following removal of the  plaster cast, a custom rocker-sole post-op boot with an EVA shell MASS posture orthotic built in (Figure 3) on 1/28/16.  That boot caused irritation and so the design was refined and a new rocker-sole boot with an EVA shell MASS Posture orthotic fitted in the boot (Figure 4) was created and dispensed to patient on 3/4/2016.  The boot (Figure 4) was removed and replaced with a modified golf shoe boot with an EVA shell MASS Posture orthotic fitted into the boot (Figure 5), which was dispensed to the patient on 3/25/2015.  Each change of successive custom boot was modeled from a new, more aggressively captured medial longitudinal arch.  The golf shoe boot (Figure 5) was removed and replaced with an ultrahigh molecular weight polyethylene shell. MASS orthotic (O1) for use with his diabetic shoes.  O1 was dispensed and fitted on 5/6/2016 with use of a full foot lift for his left foot to compensate for the edema on his right foot.   After the edema decreased another MASS orthotic with a polyethylene shell (O2) was dispensed and fitted, for his normal tennis shoes, on 8/25/2016, along with reducing the full foot lift on his left foot.

Figure 4 Refined Custom walking boot with EVA Shell MASS Posture Orthotic.

Figure 5 Modified golf shoe boot with EVA Shell MASS Posture Orthotic.


Our patient initially presented completely insensate with diabetic neuropathy on 1/28/2016.  On 3/25/2016 the patient had regained 6/10 sensation on the right foot and 8/10 on left with the monofilament test.  On 5/6/2016 the patient had a 8/10 sensation on right foot and 10/10 on left.  It should be noted that the patient has been fully compliant keeping his diabetes in control.

Although the patient’s Charcot foot has now fully fused, the foot appears to have remodeled and partially regained the medial longitudinal arch (Figure 6).  The authors believe that this is due, at least in part, to the patient weight bearing in a MASS Posture.  No ulcers developed with the forces applied to the foot.  This is due, at least in part, to the even distribution of body weight across the plantar surface of the foot.  

Figure 6 Clinical view of foot after treatment.

The patient is leading a normal life that includes golf and walking approximating an ideal gait cycle on both hard flat surfaces (hardwood) and uneven flexible surfaces (grass).  


For peripheral neuropathy, it is common conventional wisdom that only the levels of Hgb A1C correlate to the presence of neuropathy.  This particular case, along with previous findings of Michael Graham, suggest that there is a secondary biomechanical etiology that may contribute to Diabetic Peripheral Neuropathy (DPN).  Michael Graham showed that reversing neuropathy could be obtained by reducing tension on the neurovascular bundle and the intracompartmental pressures of the posterior tibial nerve utilizing an extra osseous talotarsal implant [2].  This helps explain why some diabetics with equally poor Hgb A1C’s develop DPN but others do not. The biomechanical factor is postulated to involve the mechanical elongation of the perineurium surrounding the posterior tibial nerve.  As the foot drops in posture, the neurovascular bundle is pulled plantarly increasing tension due to elongation [3].  This may cause the perineurium to compress the nerve while increasing fluid pressure within the sheath, contributing to its loss of function.


The authors postulate that using MASS Posture orthotics in combination with controlling diabetes may prevent or, in some cases reverse, diabetic neuropathy by reposturing the foot and thereby decreasing nerve tension and entrapment while evenly distributing the force from the body across the entire plantar surface of the foot.  Additionally, the authors postulate that it is possible during active Charcot to remodel the medial longitudinal arch closer to an idealized foot posture.  Further research is required with an established protocol prior to treatment with a larger sample size to provide more data to verify results.


  1. Smieja, M., Hunt, D. L., Edelman, D., Etchells, E., Cornuz, J., Simel, D. L. and For The International Cooperative Group for Clinical Examination Research (1999), Clinical Examination for the Detection of Protective Sensation in the Feet of Diabetic Patients. Journal of General Internal Medicine, 14: 418–424. 
  2. Graham ME, Jawrani NT, Goel VK. The Effect of HyProCure® Sinus Tarsi Stent on Tarsal Tunnel Compartment Pressures in Hyperpronating Feet. The Journal of Foot and Ankle Surgery. 2011;50(1):44-49. 
  3. Graham ME, Jawrani NT, Goel VK. Evaluating Plantar Fascia Strain in Hyperpronating Cadaveric Feet Following an Extra-osseous Talotarsal Stabilization Procedure. The Journal of Foot and Ankle Surgery. 2011;50(6):682-686. 

Bilateral Charcot neuroarthropathy, a challenge for diagnosis and treatment

by Nathalie Denecker1*, Dimitri Aerden2, Michel De Maeseneer3pdflrg

The Foot and Ankle Online Journal 9 (1): 6

Charcot neuroarthropathy is a devastating foot disorder whose differential diagnosis with infectious, bone or articular disease is difficult. We report a rare case of a woman with diabetes who developed bilateral Charcot neuroarthropathy after erysipelas of her left leg and subsequent trauma, which complicated diagnosis as well as efficient off-loading.

Key words: bilateral Charcot foot, diabetic foot, diabetic neuropathy, off-loading

ISSN 1941-6806
doi: 10.3827/faoj.2016.0901.0006

1,2 – UZ Brussel, Diabetic foot clinic, Laarbeeklaan, 101, 1090 Brussel, BELGIE
3 – UZ Brussel, Radiology department Laarbeeklaan, 101, 1090 Brussel, BELGIE
* – Correspondence: Nathalie Denecker nathalie.denecker@uzbrussel.be

Charcot neuroarthropathy (CN) of the foot is a rare but debilitating disorder that affects bones, joints and soft tissues and leads to significant deformity unless diagnosis is established early. We report a case of bilateral synchronous CN that proved particularly challenging because diagnosis was obfuscated 1) by bilateral symptomatology and 2) a preceding erysipelas. In addition, we had no prior experience in off-loading both limbs simultaneously.

Case report

A 58-year old woman with insulin dependent type 2 diabetes and lower limb neuropathy presented to the emergency department with fever and erythema of the left leg. The limb was erythematous and warm with a plantar neuropathic ulcer on the left hallux. Distal pulses were detected bilaterally. Blood sampling showed overt inflammation. The diagnosis of erysipelas was established with the toe ulcer as entry point. A wound smear revealed Pseudomonas aeruginosa for which intravenous antibiotics were administered for 8 days. She returned with increased oedema and pain of her leg two weeks later, although inflammatory blood parameters had normalised.

Ten days later inflammatory symptoms had persisted and spread to the contralateral foot and ankle: both feet now were swollen, red and warm, and some bruises from a recent trauma were detected. X-rays of both feet were normal. A bone scintigraphy with SPECT-CT (Single Photon Emission Computed Tomography) was suggestive for CN of both feet, with tracer uptake in the midfoot (Figure 1a) and small bony fragments on CT (Figure 1b). Hotspots over the 2nd metatarsal heads bilaterally raised the possibility of underlying osteomyelitis.

Bilateral immobilization with total contact casts (TCC) was deemed impracticable. Hence, the left foot was treated with a removable air-cushioned cast (Aircast®) but this required the patient to be hospitalized. Oedema of the tarsus and metatarsal bases shown on magnetic resonance imaging (MRI) confirmed bilateral CN (Figure 2a) but osteomyelitis of the 2nd metatarsal head was rejected by leucocyte scan with SPECT-CT. Transfer to a rehabilitation centre and regular ambulatory appointments to renew the TCC were initiated. Three months later clinical inflammatory signs and oedema of the midfoot on control MRI had decreased, although increased oedema was observed at the talar bone bilaterally (Figure 2b). Off-loading was continued with bilateral Aircast® walkers for another 3 months until orthopaedic shoes became available. Final ambulatory rehabilitation was satisfactory.


Figure 1 (a) Bone scintigraphy shows tracer uptake in the midfoot and 2nd metatarsal heads bilaterally. (b) Irregular margins and bone fragments in the midfoot are seen on SPECT-CT.


Charcot neuroarthropathy or Charcot foot is a devastating complication of neuropathy which is mostly seen as a rare complication of longstanding diabetes [1-5]. Men and women are equally affected [2,6]. Until recently, the prevailing hypothesis for pathogenesis was neurotraumatic or neurovascular [2,7,8]. Authors have observed however that CN is also associated with an enhanced inflammatory response, presumably triggered by minor trauma, prior infection, ulceration or foot surgery. Pro-inflammatory cytokines (TNF-α, IL-1ß) are released and lead to increased expression of receptor activator of nuclear factor-κB (RANK) ligand, thereby activating NF-κB (Nuclear Factor κB), a potent promotor of osteoclastic activity which promotes osteolysis and fractures [1,2,8,9].

The prevalence of CN is underestimated but affects less than 1% of all patients with diabetes [6,8-10]. Moreover, local inflammation is inhibited by limited arterial inflow, a frequent occurrence in patients prone to macrovascular disease [9]. Ipsilateral recurrence of CN is rare [10]. Over several years, contralateral CN may occur in 20% to 30% [6,7,11]. Off-loading of the index foot has been suggested as the initiating event that may develop CN at the contralateral foot [11].


Figure 2 (a) MRI of the right foot initially shows bone marrow oedema of the tarsus and metatarsal bases. (b) Three months later oedema in the original regions has improved but is now more prominent in the talar bone.

Diagnosis of acute Charcot foot is primarily established clinically because no specific laboratory tests are available: a unilateral red, warm, swollen foot that is remarkably painless due to neuropathy. Differential diagnosis should be made with infection (cellulitis, osteomyelitis, arthritis, abscess), acute gout, deep venous thrombosis and trauma (sprain, fracture) [1-4,11,12]. Imaging techniques are helpful but X-rays lack sensitivity during the first weeks. The sensitivity of bone scintigraphy is superior and its low specificity is improved by SPECT-CT. MRI has diagnostic accuracy in the early stages and allows differentiation from osteomyelitis [1-3,11]. According to literature, the diagnosis of CN may be missed in 79% and delayed up to 29 weeks [11]. Unfortunately, early recognition of CN and prompt treatment is mandatory to prevent foot deformation.

Rapid immobilisation of the affected foot is paramount and accomplished best by TCC, the gold standard for off-loading [1,13]. A removable pneumatic walker achieves comparable off-loading but non-compliance remains a problem [4,10]. Immobilisation is advised until clinical signs have resolved and a temperature difference of <2°C between feet is recorded [1,9,14]. In general, this occurs after 3-12 months, with 6 months being most common [10,11,14]. Bisphosphonates which inhibit bone resorption have been suggested as adjunctive therapy but current data do not support their routine use [5].

Bilateral synchronous CN as reported in the presented case is not only an extremely rare occurrence, but also greatly complicates diagnosis and subsequent immobilisation/off-loading. To our knowledge, only one similar case has previously been reported: a man in which contralateral CN presumably was elicited two weeks after off-loading his index foot with a TCC [12]. In our case, a skin infection probably triggered CN on the index side which unfortunately also delayed diagnosis. On the contralateral side both the overloading of the right foot due to pain on the left side, or trauma may have been the trigger for CN. The number of radiological exams that had to be performed, and their conflicting findings demonstrate how difficult a diagnosis can be. Long-term immobilisation and off-loading of both limbs was extremely debilitating to our patient and justified hospitalisation in a rehabilitation centre.

In summary, diagnosis of acute Charcot foot is challenging, especially when triggered by prior infection or trauma. Bilateral CN, although extremely rare, further complicates the diagnosis as well as efficient off-loading and immobilisation.


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