Risk of relapse of Guillain-Barré syndrome or chronic inflammatory demyelinating polyradiculoneuropathy following immunisation.

oligoclonal bands were not found. DNA was extracted from a blood sample and analysed for mtDNA mutations using standard procedures and was negative at positions 3243, 8344, 8993, 3460, and 14484, but with a homoplasmic mutation at position 11778. Our patient had the mutation most often associated with MS-like CNS lesions and visual loss in women. Brain stem lesions have been previously described in a patient with visual loss, complete ophthalmoplegia, and bilateral tinnitus. However, to our knowledge, this is the first description of LHON in association with brain stem lesions presenting with respiratory arrest and loss of involuntary ventilation (Ondine’s curse). The high signal lesions in the pons and medulla involved the nucleus ambiguus and nucleus of the solitary tract, which are part of the ventral and dorsal respiratory groups respectively, and would seem well placed to account for loss of respiratory control during sleep with well preserved capacity for volitional respiratory manoeuvres while awake. Ondine’s curse produced by lesions of these structures and their tracts through a variety of causes has been well described. 5 However, the exact nature of CNS lesions in patients with mitochondrial cytopathy remains obscure. Our patient tolerated NIPPV. She improved on this regimen such that 123 days after admission she was able to take a 45 minute daytime nap and maintain an oxygen saturation of >97% throughout, while breathing room air unassisted. Eight months after her respiratory arrest, she was able to take a few steps with a Zimmer frame and had successfully weaned off NIPPV support. This patient provides a further example of the broad manifestations of mitochondrial disease.