Charcot spine: a complication of medullary arteriovenous malformation

Vialle, Raphaël; Parker, Fabrice; Lepeintre, J.-F.; Rodesch, Georges; Tassin, Jean-Louis; Tadié, M

doi:10.3171/spi.2004.1.1.0141

Cited by 3 publications

(2 citation statements)

References 5 publications

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“…Late-stage SNA closely mimics several other spinal conditions, most importantly spinal infection. The overlap of imaging and clinical features with those of other spinal pathologic conditions, particularly spinal infection, creates a diagnostic disease, Guillain-Barré syndrome, transverse myelitis, and Friedreich ataxia (10)(11)(12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Spinal Neuroarthropathy: Pathophysiology, Clinical and Imaging Features, and Differential Diagnosis

Ledbetter

Rk³

et al. 2016

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Spinal neuroarthropathy (SNA), or Charcot spine, is a progressive destructive arthropathy occurring after loss of neuroprotective sensation and proprioceptive reflexes. Clinical diagnosis is difficult because of the variable length to presentation after initial neurologic damage and the limited symptoms given preexisting neurologic deficits. SNA is also a diagnostic challenge because its imaging features are similar to those of spinal conditions such as discitis-osteomyelitis, osseous tuberculosis, hemodialysis-related spondyloarthropathy, and pseudarthrosis. The most important imaging clues for diagnosis of SNA are involvement of both anterior and posterior elements at the thoracolumbar and lumbosacral junctions. Additional imaging clues include vacuum phenomenon within the disk (indicating excessive motion), malalignment, and paraspinal soft-tissue masses or fluid collections containing bone debris. Despite these imaging signs, findings may overlap in some cases with those of infection, or SNA can be superinfected, and biopsy may be necessary. Development of SNA requires a preexisting neurologic condition, most commonly traumatic spinal cord injury. Areas of greatest mobility and weight bearing within the desensate spine experience repetitive microtrauma and unregulated hyperemia, leading to destruction of the intervertebral articulations. The progressive and destructive nature of SNA causes substantial deformity, loss of function, and often further neurologic deficits. Patients present with deformity, back pain, audible noises during movement, or new neurologic symptoms. The mainstay of treatment is surgical débridement, reduction, and fusion. The radiologist can help initiate early intervention by using key imaging features to distinguish SNA from imaging mimics and prevent further neurologic deterioration. (©)RSNA, 2016.

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Section: Introductionmentioning

confidence: 99%

Spinal Neuroarthropathy: Pathophysiology, Clinical and Imaging Features, and Differential Diagnosis

Ledbetter

Rk³

et al. 2016

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“…3,7,10,11,17,23,[35][36][37][38][39][40][41] Other less common conditions associated with CSA include diabetic neuropathy, syringomyelia, meningocele, myelomeningocele, anesthetic leprosy, congenital insensitivity to pain, medullary AV malformation, Parkinson's disease, transverse myelitis, Guillain-Barré syndrome, Friedreich ataxia, Charcot-Marie-Tooth disease, arachnoiditis, and others. 3,12,19,39,[42][43][44][45][46][47][48][49][50] Unfortunately, the incidence and prevalence of CSA are difficult to determine since CSA has been reported largely in case reports and small case series. The estimated prevalence of CSA developing after SCI is 1 in 220, and the incidence and prevalence of SCI in the United States (US) are 54 per 1 million (17,700 cases per year) and 288,000, respectively.…”

Section: Epidemiologymentioning

confidence: 99%

A comprehensive review of the treatment and management of Charcot spine

Urits

Amgalan

Israel

et al. 2020

Therapeutic Advances in Musculoskeletal

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Charcot spine arthropathy (CSA), a result of reduced afferent innervation, is an occurrence of Charcot joint, a progressive, degenerative disorder in vertebral joints, related mostly to spinal cord injury. The repeated microtrauma is a result of a lack of muscle protection and destroys cartilage, ligaments, and disc spaces, leading to vertebrae destruction, joint instability, subluxation, and dislocation. Joint destruction compresses nerve roots, resulting in pain, paresthesia, sensory loss, dysautonomia, and spasticity. CSA presents with back pain, spinal deformity and instability, and audible spine noises during movement. Autonomic dysfunction includes bowel and bladder dysfunction. It is slowly progressive and usually diagnosed at a late stage, usually, on average, 20 years after the first initial insult. Diagnosis is rarely clinical related to the nature of nonspecific symptoms and requires imaging with computed tomography (CT) and magnetic resonance imaging (MRI). Conservative management focuses on the prevention of fractures and the progression of deformities. This includes bed rest, orthoses, and braces. These could be useful in elderly or frail patients who are not candidates for surgical treatment, or in minimally symptomatic patients, such as patients with spontaneous fusion leading to a stable spine. Symptomatic treatment is offered for autonomic dysfunction, such as anticholinergics for bladder control. Most patients require surgical treatment. Spinal fusion is achieved with open, minimally-open (MOA) or minimally-invasive (MIS) approaches. The gold standard is open circumferential fusion; data is lacking to determine the superiority of open or MIS approaches. Patients usually improve after surgery; however, the rarity of the condition makes it difficult to estimate outcomes. This is a review of the latest and seminal literature about the treatment and chronic management of Charcot spine. The review includes the background of the syndrome, clinical presentation, and diagnosis, and compares the different treatment options that are currently available.

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