A case of charcot's feet in a patient with parkinson's disease: a case report
© Singh and Kelly; licensee BioMed Central Ltd. 2009
Received: 19 October 2009
Accepted: 09 November 2009
Published: 09 November 2009
Parkinson's Disease (PD), amongst its motor symptoms, can cause dystonia of the limbs and trunk. This can lead to subsequent deformities.
We describe a case where Parkinson's Disease has gone on to cause bilateral Charcot feet with rocker-bottom deformity.
There is recognised pattern of foot deformities seen in Parkinson's disease and it is important to realise that patients may go on to develop a Charcot joint. This would warrant early referral to an orthopaedic surgeon so that appropriate management can limit joint damage and deformity.
Charcot's arthropathy is a progressive condition characterized by joint destruction, debilitating deformities and pathological fractures. Though it can occur at any joint, it is most commonly seen in the lower extremity, at the foot and ankle. Historically the most common cause was syphilis but diabetes is now the most common aetiology. The major theories to explain Charcot joints are the Neurotraumatic and Neurovascualar theory. The first suggests that the arthropathy is caused by unperceived trauma in an insensate foot and the latter, that there is an autonomic neuropathy causing a mismatch in bone destruction and synthesis. Amongst its other complications, Charcot arthropathy can lead to midfoot collapse and inversion of the plantar arch leading to a rocker-bottom foot deformity .
James Parkinson first described the symptoms of the "shaking palsy" in 1812. Unfortunately, Parkinson made no mention of the rigidity or the mask like facies. It was Jean-Martin Charcot, who felt that Parkinson was the crucial pioneer and named the condition "Maladie de Parkinson." He favoured this over the original name "Paralysis Agitans" [2, 3].
Hyperextension of the hallux
Clawing of the lesser toes
These deformities where placed under the phrase "striatal foot" by Charcot. The term "striatal" being used as it referred to pathology in the neostriatum which was suggested to be the cause. Early reports attributed the postural abnormalities to muscular rigidity but subsequent studies suggest an extrapyramidal origin. Dystonias associated with PD can affect the hand, feet, trunk (camptocormia), head (anterocollis) and cause scoliosis. There are many theories as to the cause of these dystonias, such as damage to the striatopallidothalamic pathway, caudate nucleus, globus pallidus and putamen. The exact mechanism, however, is unclear .
Our patient has no evidence of diabetes mellitus and had an EMG to exclude a peripheral neuropathy. She also did not have the typical deformities seen in PD. We postulate that the dystonia, as a result of her PD, would have resulted in altered feet posture and gait. The subsequent altered mechanics may have caused abnormal stresses in the joints and the resulting trauma initiated the Charcot arthropathy.
Though there is recognised pattern of foot deformities seen in Parkinson's disease, it is important to realise that such patients may go on to develop a Charcot joint. This would warrant early referral to an orthopaedic surgeon so that appropriate management can be put in place to prevent or limit joint damage and deformity. We would aim to limit functional disability in patients already coping with PD symptoms.
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
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