Gadolinium-enhancement of the spinal posterior roots in acute sensory ataxic neuropathy
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Acute sensory ataxic neuropathy (ASAN) is characterized by the acute onset of sensory ataxia and areflexia.1 The persistent neurologic deficit, absence of sensory nerve action potentials, and loss of large myelinated fibers in sural nerve biopsy could be explained by an immune-mediated or vascular process at the level of the posterior root or dorsal root ganglion (DRG).1 An autopsy study in an ASAN patient with minimal autonomic dysfunction showed T-cell-mediated ganglionitis.2 However, the site of the lesion has remained obscure in ASAN without autonomic dysfunction. Here we report the visualization of the lesion in the posterior roots of the spinal cord in an ASAN patient without autonomic dysfunction.
Case report. A 70-year-old woman had been in good health until she presented with an acute onset of progressive sensory disturbance of her limbs and unsteady gait after an antecedent episode of upper respiratory tract infection. The sensory disturbance appeared at first in the left upper limb and then spread …
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