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Richard Leblanc

-Martin Charcot 2 and his student Albert Pitres 3 in a more serene atmosphere, through 3 papers published between 1877 and 1879 and 2 books published in 1883 and 1895. 4–8 This paper describes Charcot and Pitres' discovery of the human cortical motor zone and its somatotopic organization, and argues that they played a determining role in the origins of 19th-century neurosurgery. Methods Charcot and Pitres' publications on motor localization, and those of others written in French on the same topic, have been consulted and pertinent passages translated into English for

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Masahiro Morita, Akira Miyauchi, Shinya Okuda, Takenori Oda, Tomio Yamamoto, and Motoki Iwasaki

T he pathological mechanisms underlying Charcot arthropathy are believed to involve repetitive minor trauma to joints that have lost protective mechanisms due to the destruction of afferent proprioceptive fibers caused by primary disease such as diabetic neuropathy, tertiary syphilis, anesthetic leprosy, syringomyelia, congenital absence of pain syndrome, or SCI. 9 Destruction of all 3 columns of the spine can also generate CSD (also called neuropathic spinal arthropathy). Most reports in the earliest literature of CSD involved patients with tabes

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Joseph Hong, James A. Sanfilippo, Jeffrey Rihn, Carmella Fernandez, Corbett D. Winegar, Brian Friel, Steven Ludwig, Daniel Gelb, and Alexander R. Vaccaro

T he inability to restore or maintain stability and alignment following decompressive laminectomy and/or fusion procedures in the face of Charcot spinal arthropathy can result in poor functional outcomes. The insensate nature of the vertebral elements above and below the fused segments leads to repetitive microtrauma and inflammation, which causes a vicious cycle of progressive deformity, tissue destruction, pseudarthrosis, and worsening instability. 3 Historically, the etiology of Charcot spine has included patients with SCI from traumatic causes as

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Marcus de Matas, Peter Francis, and John B. Miles

, Meaney JFN, et al: Coexistent trigeminal neuralgia, hemifacial spasm and hypertension: preoperative imaging of neurovascular compression. Case report. J Neurosurg 80: 559–563, 1994 2. Braga FM , Bonatelli AP , Suriano I , et al : Familial trigeminal neuralgia. Surg Neurol 26 : 405 – 408 , 1986 Braga FM, Bonatelli AP, Suriano I, et al: Familial trigeminal neuralgia. Surg Neurol 26: 405–408, 1986 3. Chance PF , Pleasure D : Charcot-Marie-Tooth syndrome. Arch Neurol 50 : 1180 – 1184 , 1993 Chance PF, Pleasure D: Charcot-Marie-Tooth syndrome

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Frank S. Bishop, Andrew T. Dailey, and Meic H. Schmidt

C harcot disease of the spine, also known as spinal neuropathic or neurogenic arthropathy, is a destructive degenerative process involving the vertebral bodies and surrounding discs. This condition results from repetitive microtrauma in patients who have decreased joint protective mechanisms from loss of deep pain and proprioceptive sensation, typically because of spinal cord injury or sensory neuropathies. The patient typically presents with back pain and progressive spinal instability and deformity. We report a unique case of massive Charcot spinal disease

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A. Alex Mohit, Sohail Mirza, Jennifer James, and Robert Goodkin

N europathic spinal arthropathy represents a mechanical joint degeneration that occurs as a result of impaired deep sensation to facet joints. Although initially described by Mitchell, 20 it is commonly referred to as a Charcot joint, after Charcot described its association with tabes dorsalis. In 1884, Kronig 16 was the first to describe its manifestation in the spinal column. Today, neuropathic spinal arthropathy is more commonly encountered as one of the sequelae of spinal cord injury. Rare reports describe its occurrence in patients with diabetes

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Nissim Ohana, Daniel Benharroch, and Dimitri Sheinis

C harcot spinal arthropathy (CSA), also called neuropathic spinal joint disorder (Charcot spine), is a rare destructive medical condition secondary to a local innervation deficit, mainly resulting from a persistent paralysis of the limbs subsequent to traumatic damage to the spine. A pseudarthrosis follows distally to the fixed segment of the spine. 4 , 12 The CSA is considered the late sequel of old traumatic damage progressing to a degenerative lesion, highlighted by a lack of proprioceptive sensation and occurring rarely in paralyzed and mainly in paraplegic

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W. Bradley Jacobs, Richard J. Bransford, Carlo Bellabarba, and Jens R. Chapman

. Inclusion and Exclusion Criteria Inclusion in the study was determined via a search of the University of Washington Spine Registry for patients who had undergone surgery between January 1997 and January 2009 and had received a primary diagnosis of “Charcot spinal arthropathy,” “neuropathic spinal arthropathy,” or “spinal neuroarthropathy,” or had the ICD-9 code 713.5 (arthropathy associated with neurological disorders). Patients were subsequently excluded from the study cohort if, on our review of hospital records and/or radiographic images, their diagnosis was deemed

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Dilantha B. Ellegala, Stephen J. Monteith, David Haynor, Thomas D. Bird, Robert Goodkin, and Michel Kliot

C harcot-Marie-Tooth disease is one of the most common genetically transmitted diseases with an estimated incidence of one in 2500 individuals. First described in 1886 by Jean Martin Charcot and Pierre Marie at the Hopital de la Salpetriere in Paris and separately in the same year by Howard Henry Tooth at Cambridge, this group of disorders is characterized by distal muscle weakness and atrophy, impaired sensation, and diminished deep tendon reflexes. Specifically, there is tibialis anterior and peroneal muscle wasting with later development of weakness in the

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Day P. McNeel and George Ehni

H istorically , the relationship between spinal cord lesions and certain joint diseases is well recognized, having been pointed out by Mitchell in 1831. Later, neurogenic arthropathies were observed in hemiplegia by Scott and Allison in 1843, in syringomyelia by Blasius in 1848, in acute myelitis by Magnier in 1859, and in relation to lesions of peripheral nerves by Packard in 1861 (described by Delano). 6 Following Charcot's description in 1868 9 of joint changes in tabetics, neurogenic arthropathies became known as “Charcot joints.” Jordan in 1936 15