We present the case of a 10-year-old boy with no past history of interest, with bilateral gonalgia, back pain and low back pain after a fall from a bicycle 4 days ago. On examination he had preserved active and passive mobility with pain in both lower limbs (MMII). There were no signs of fractures or neurological alterations. Rest, local cold and anti-inflammatory treatment was prescribed. After 48 hours, the patient returned for persistent pain, loss of strength, paresthesia in the lower limbs, difficulty in standing and walking and urinary incontinence. Physical examination revealed a decrease in strength and altered sensation in both LMMII. Suspecting transverse myelitis, the patient was referred to the hospital emergency department. On admission, blood tests were normal, the cerebrospinal fluid study revealed moderate pleocytosis, without the presence of oligoclonal IgG bands; the electroencephalogram showed no alterations and the evoked potentials showed paralysis and spasticity of MMII, hyporeflexia and bilateral Babinsky, absence of abdominal and cremasteric reflexes, hyperalgesia and dysaesthesia of the trunk and MMII. Electromyogram revealed impaired medullary somatosensory sensation through the posterior cords, with no conduction through the right cord and partial impairment of the left cord. Magnetic resonance imaging (MRI) of the brain was normal, however, spinal MRI showed an expansive lesion at spinal cord level from D1 to D6 compatible with transverse myelitis.

Twenty-four hours after admission, the patient presented intense pain in the right eye with sudden loss of visual acuity. He was assessed by ophthalmology and a diagnosis of right optic neuritis was made.
In view of the presence of transverse myelitis and optic neuritis, with brain MRI that did not meet multiple sclerosis criteria and spinal MRI showing a lesion of three or more spinal segments (D1 to D6), an anti-acuoporin-4 antibody test was performed, which was negative. Based on the clinical manifestations, evolution and despite the negative antibody, the patient was diagnosed with neuromyelitis optica or Devic's disease (see diagnostic criteria table 1).

The patient was initially treated with intravenous methylprednisolone at a dose of 1 g/day without improvement, so plasmapheresis was performed with good clinical evolution.
The patient was followed up by neurology, ophthalmology and urology with progressive improvement and progressive decrease of corticotherapy. Fourteen months later, the patient presented complete recovery of strength and sensitivity of the lower limbs, normal gait, normal reflexes, absence of spasticity, ataxia or dysmetria; occasionally he presented painful lumbar hyperaesthesia of a self-limited nature. In the right eye, he maintained blurred near vision, with attenuation of colour perception, although he managed to recover 70% of visual acuity. Nocturnal enuresis persists due to bladder spasticity, which continues to be treated with desmopressin.