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30 Examining the neuroanatomical pathology of post-stroke apathayuthors
  1. Joseph Lam,
  2. Dennis Minioza,
  3. Himanshu Tyagi
  1. Neurorehabilitation Unit, National Hospital of Neurology and Neurosurgery, Queen Square, University College London Hospital NHS Foundation Trust, WC1N 3BG


Objectives Apathy has been associated with frontal-subcortical pathway impairments. However, presentation of apathy and its subtypes (e.g. behavioural, cognitive, executive, social) differs amongst neurological and psychiatric disorders. Our review focused on the neuroanatomy of apathy following acquired brain injury (stroke and traumatic brain injury (TBI)), with an aim to identify unique and shared neural networks underlying apathy presentation in different disorders. We aim to demonstrate a visual overview of the identified locations, types of lesion and neural pathways associated with apathy.

Methods We explored peer-reviewed literature from Web of Science, PubMed and Psychinfo. Imaging studies looking at the association between brain lesion location and apathy symptoms in post-stroke or TBI patients were reviewed. A series of brain images would be used to depict the neural network of motivation in a healthy brain versus an apathetic brain. Identified regions of impairments related to apathy would be presented separately for TBI and stroke patients. We would further describe the association between stroke types and apathy.

Results MRI studies consistently show that apathy appears related to impairments at the frontal-subcortical circuit. Apathy appeared to be more prevalent following lacunar stroke, with lesions at subcortical areas such as the pons and anterior cingulate cortex. Rate of apathy appears to be similar across ischemic and haemorrhagic stroke. Previous reviews did not identify an association between stroke volume with post-stroke apathy. Recent research explored the relationship between white matter microstructure reduction with post-stroke apathy without identifying any specific correlation with lesion locations.

Conclusions Post-TBI apathy is highly prevalent yet under-researched. Evidence regarding the location of lesions was less consistent for post-stroke apathy. Due to the widespread use of apathy scales that do not specify subtypes, the current review could not speculate the relationship between brain injury with specific apathy subtype presentations. Null finding in previous reviews regarding lesion size and location could be potentially attributed to the poor differentiation amongst apathy subtypes.

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