This case was reported in a literature article and described the occurrence of multiple sclerosis in a 11-year-old female subject who was vaccinated with DTPa (with small D + P), manufacturer unspecified), Meningococcal polysaccharide vaccine (non-GSK) and HPV vaccine. The subject was reported to be healthy before the event. She had no previous history of viral illness. No further information regarding the subject's medical history, concurrent medical conditions or concomitant medication was provided. On an unspecified date the subject received unspecified dose of DTPa (with small D + P) (administration site and route unknown, batch number not provided), an unspecified dose of Meningococcal polysaccharide vaccine (non-GSK) (administration site and route unknown, batch number not provided) and an unspecified dose of HPV (administration site and route unknown, batch number not provided). 2 weeks after vaccination with DTPa (with small D + P), Meningococcal polysaccharide vaccine group C (non-GSK) and HPV vaccine, the subject started developing double and blurry vision that was noted upon awakening and that was associated with intermittent hypogeusia and emotional lability. Upon examination 2 weeks after the onset of the symptoms she was found to have bilateral ptosis and large angle exotropia in primary gaze (approximately a 15 degree chin-up position). She had reduced ocular motility with no vertical movements bilaterally, only 10% of adduction in each eye, as well as normal lateral rectus and superior oblique functions with bilateral intorsion on attempted downgaze. In addition to this, her near visual acuity was decreased (20/400 OD and 20/200 OS at 12-154 inches) and her colour vision was reduced in both eyes (2 of 8 Ishihara plates OD and 4 OS). Six months after the first admission, the subject was readmitted with confusion, ataxia, dysarthria and nystagmus. The subject was hospitalised. Further investigations during the first admission included pupils examinations (diameter: 4mm in light and 6.5 mm in dark, moderate reaction to light stimulation without an efferent pupillary defect); dilated fundus examination (normal discs, vessels, maculae and peripheral retinae) and neurological examination that was normal. A contrast brain MRI revealed multiple T2/FLAIR hyperintensities scattered throughout the white matter, with involvement of the basal ganglia, frontal periventricular area and midbrain. Full blood count, biochemistry test, erythrocyte sedimentation rate and Lyme immunoglobulin G/M were normal. Lumbar puncture revealed normal opening pressure, protein, glucose and 4 white blood cells. Myelin basic protein and oligoclonal bands were not performed due to inadequate cerebrospinal fluid sample volume. An electroencephalogram showed epileptiform activity and focal slowing over both frontal lobes without evidence of clinical seizure. An MRI performed during the second admission revealed new T2/FLAIR hyperintensities localised to bilateral internal capsules, bilateral cerebral peduncles and left pons. An increase in the size and intensity of bilateral periventricular white matter lesions was also noted. Anti-neuromyelitis optica antibodies were not analysed but cervical and thoracic spine MRI results were normal. Repeat cerebrospinal fluid studies were within normal limits with respect to opening pressure, protein, glucose, white cell count, immunoglobulin G index and myelin basic protein. However, cerebrospinal fluid oligoclonal bands disclosed 45 gamma restriction bands that were not present in the subject's serum. Visual acuities were 20/20 OU with normal colour vision and ocular motility. The only abnormal finding on neuro-ophthalmic examination at this time was a mild left beating, horizontal nystagmus worse in right gaze. Due to bilateral oculomotor nerve palsies without pupillary involvement and bilateral optic neuropathy, pediatric multiple sclerosis was diagnosed. During the initial admission the subject was treated with intravenous methylprednisolone (1 mg/kg) and a loading dose of IV levetiracetam due to the electroencephalogram findings. She received a 5-day course of pulsed intravenous methylprednisolone (800 mg daily) during the second admission, and she was then placed on a slow taper of oral prednisone. She was scheduled for outpatient paediatric neurology and neuro-ophthalmology outpatients review but she was lost to follow up. The outcome of the diplopia in primary gaze and decreased colour vision was resolution after 6 days of intravenous treatment and by the first discharge respectively. The ptosis, ocular motility, visual acuity problems had improved by the time of the first discharge and had resolved by the second admission. The outcome of the hypogeusia, emotional lability, confusion, ataxia. dysarthria and nystagmus was unspecified at the time of reporting. The authors did not comment on any possible causal relationship between the events and the vaccinations. The authors' conclusion stated that when faced with a subject demonstrating new onset bilateral ophthalmoplegia, a thorough ophthalmological and neurological examination, and prompt laboratory and imaging workup, as essential to rule out underlying primary diagnoses with high potential for significant morbidity and mortality. The article corresponding to this case is not available for submission due to copyright restriction.