A 34 year-old, right-handed, mother of two was at home one evening when she walked into a door-frame, hitting her left temple. The next morning she continued to bump in to objects on her left and was beginning to drag her left leg. She noticed she was dropping items and that her right arm was clumsier than normal. As the day progressed her left leg became weaker as well. There was no headache, vomiting or malaise but she had recently recovered from a minor viral illness. She had worked as a hairdresser, but retired to care for her eldest child who has cerebral palsy. Her only regular prescribed medication was citalopram for depression.

On examination she had corticobulbar dysarthria, left hemiparesis, left homonymous hemianopia and left visual inattention. There was ataxia of the right upper limb. There were no other abnormalities on examination; in particular she did not have optic atrophy nor an internuclear ophthalmoplegia.

COMMENT

Many of her signs suggest a right hemisphere process; the left hemiparesis, homonymous hemianopia and visual inattention are all consistent with this. But is this a diffuse cortical lesion or a more localised thalamic lesion? The thalamus is recognised as producing pseudo-cortical symptoms and signs. And is the lesion entirely consigned to the right hemisphere? How could a single right cortical lesion produce a right-sided ataxia without extension into the brain stem? Perhaps there are two lesions, or more?

MR imaging of the brain confirmed a large subcortical parieto-occipital hyperintense lesion in the right hemisphere (fig 1) involving the right lateral thalamus, compatible with demyelination. The lesion appears to creep across the corpus callosum, hinted at in fig 1A.