A Closer Look At Redefining Charcot

By Molly Judge, DPM

   For foot and ankle specialists, the diagnosis and complete management of neuropathic arthropathy ranks among the most daunting challenges. Currently, one makes the clinical diagnosis when there is a compilation of clinical and radiographic findings suspicious for the condition. The diagnosis relies upon the histopathology to identify the neuropathic joint destruction.

   Once one makes a diagnosis, either definitively or clinically, the treatment approach remains the discretion of the physician. Those best trained for treating this condition rely on the literature completed by some of the world’s most renowned authorities in the fields of diabetes research and foot and ankle surgery.1 Although there are numerous articles on managing the condition, many are case reports and isolated accounts of individual experience.2 The traditional academic approach considers the etiology of Charcot neuroarthropathy, possible triggers of the disease process and focuses on arresting the acute, destructive phase of this condition.

   While there are numerous conditions that lend themselves to the development of neuroarthropathy, the prevailing thinking is there are at least two essential components that incite neuropathic joint destruction: a significant sensory nerve deficit (somatic and autonomic); and trauma (trivial or otherwise).3

Understanding The Degenerative Changes With Neuropathic Joints

   The historical literature reveals significant insight regarding the neuropathic joint and how it behaves. In 1917, Eloesser designed animal research testing to answer critical questions regarding how and why a neuropathic joint undergoes degenerative changes.4 One of the first questions he posed was: Is a nerve lesion the primary cause of Charcot joint? For example, does a degenerative change in nerve result in bone atrophy?

   To study this, he sectioned a dorsal nerve root to the extremity in 42 cats, producing total analgesia, anesthesia and ataxia in a unilateral fashion. Each animal developed a degenerative posterior column, producing unilateral neuropathy and allowing for the contralateral limb to serve as a control. All animals developed ataxia, hypotonia in gait and loss of pain perception.

   Seventy percent developed spontaneous lesions of bone including multiple fractures and dislocations while 30 percent developed typical Charcot joint changes. While nerve damage produced a dysfunctional limb, this study did not identify the cause of the Charcot joint.4

   These findings only prompted further questions. Is the Charcot joint the result of trophic bone changes due to a nerve lesion or is it the result of abnormal movements of ataxia in an anesthetic limb?

   Eloesser studied this question in two parts. First, he looked at the ribs of normal controls and denervated cats. In vitro chemical analysis and stress studies of the ribs failed to reveal evidence of atrophy or weakness on these non-weightbearing bones. These findings seem to discount the theory of Charcot that a trophic nerve disturbance resulted in the wasting of bone.4

   Eloesser further noted in stress testing the ribs that the affected bone was usually a little stronger than the unaffected side. He chose not to speculate if these findings were due to a trophic nerve disturbance affecting bone metabolism. He related that the denseness one sees in tabetic bone on X-ray might be the result of ataxia and loss of normal muscle function that increases weightbearing stress on bone. The experiment did not answer the question of whether trophic nerve injury itself caused bone to become more dense, sclerotic and susceptible to bone and joint damage.4

   In a subsequent phase of the experiment, Eloesser explored the question of whether it was the ataxia in an anesthetic limb that incited a Charcot arthropathy. Was it the unnatural positions assumed by the ataxic individual that resulted in fractures and dislocations?

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