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Poster abstracts
069 A putative mechanism for subcortical aphasia
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  1. Shadi El-Wahsh1,2,
  2. David Greenup3,
  3. Gemma White4,
  4. Michael J Fulham5,6,
  5. Arun Aggarwal3,7 and
  6. G Michael Halmagyi1
  1. 1Neurology, Royal Prince Alfred Hospital, Sydney, NSW, Australia
  2. 2South Western Sydney Clinical School, University of New South Wales, Sydney, NSW, Australia
  3. 3Department of Rehabilitation Medicine, Balmain Hospital, Sydney, NSW, Australia
  4. 4Speech pathology department, Balmain Hospital, Sydney, NSW, Australia
  5. 5Department of Molecular Imaging (PET and Nuclear Medicine), Royal Prince Alfred Hospital, Sydney, NSW, Australia
  6. 6Sydney Medical School, University of Sydney, Sydney, NSW, Australia
  7. 7Neurology, Concord Repatriation General Hospital, Sydney, NSW, Australia

Abstract

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.

http://dx.doi.org/10.1136/bmjno-2021-ANZAN.69

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