RT Journal Article SR Electronic T1 069 A putative mechanism for subcortical aphasia JF BMJ Neurology Open JO BMJ Neurol Open FD BMJ Publishing Group Ltd SP A25 OP A25 DO 10.1136/bmjno-2021-ANZAN.69 VO 3 IS Suppl 1 A1 El-Wahsh, Shadi A1 Greenup, David A1 White, Gemma A1 Fulham, Michael J A1 Aggarwal, Arun A1 Michael Halmagyi, G YR 2021 UL http://neurologyopen.bmj.com/content/3/Suppl_1/A25.2.abstract AB Objectives The role of subcortical structures in language function are still poorly understood. We aim to provide a putative mechanism for subcortical aphasia through a structural and functional imaging-based case discussion.Methods We present a case of subcortical aphasia due to basal ganglia hypertensive haemorrhage and discuss serial MRI and PET imaging findings to elucidate the mechanism of profound language impairment in acute subcortical pathology.Results A 71-year-old right-handed architect presented with acute onset global aphasia and right-sided hemiparesis. CT imaging showed a flame-shaped left-sided basal ganglia haemorrhage. MRI brain showed a left basal ganglia haemorrhage without ischaemic or haemorrhagic damage to the overlying fronto-parietal cortex. FDG-PET imaging showed profound left fronto-parietal cortex hypometabolism, as well as ipsilateral caudate, putamen, thalamic and pontine hypometabolism. MR tractography identified truncation of the arcuate fasciculus around the left angular gyrus as well as disconnection of the left fronto-parietal association fibres. Over 12 weeks of rehabilitation, the patient began to generate verbal output and was discharged home with ongoing word finding difficulties, nominal aphasia, and semantic paraphasias. Progress PET imaging revealed persistent hypometabolism in the aforementioned regions.Conclusion We believe this is an important educational case for neurologists regarding the presentation of aphasia due to isolated subcortical lesions and raises some interesting hypotheses regarding a putative mechanism for subcortical aphasia due to dominant hemisphere cortical inactivation.