Project Summary
Non-primary visuospatial deficits are common after right-hemisphere (RH) injury, and they are known
predictors of long-term disability after stroke. However, compared to impairments of language and motor
function, they are less obvious and receive less attention in stroke research, diagnostics, and rehabilitation,
resulting in underdiagnosis and undertreatment of RH stroke. Part of the problem is that these deficits and their
neural bases are poorly understood, not least because of the heterogeneity of the tests used to assess them
and a lack of agreement on their definition, which hamper comparison across studies.
Based on our preliminary data and a review of the literature, we posit that these deficits, which are often
subsumed under “spatial neglect”, reflect four core factors: lateralized perceptual-attentional, lateralized motor-
intentional, non-lateralized attentional, and constructional. We further posit that they can be dissociated with
appropriate assessments, are associated with different lesion sites, and respond to different treatments.
To pave the way for better assessments and effective individualized treatments, the proposed research seeks
to identify the core factors underlying visuospatial deficits, the assessments most sensitive and
specific to them, their associations with functional outcomes after stroke, and their neural bases.
SA1: Identify core visuospatial deficits and tests that are sensitive and specific to them and determine
their association with long-term stroke outcomes. Assess long-term survivors of RH vs. LH stroke and
matched Controls with a comprehensive battery of visuospatial tests. Use factor analysis to confirm that
performance is better described by a model assuming multiple different rather than one unitary underlying
deficit. Demonstrate that core deficits (captured as composite scores across battery subtests) are more severe
in RH than LH stroke, and determine which best predict functional ability and self-reported quality of life.
SA2: Identify neural bases of visuospatial deficits and their recovery. Acquire functional and anatomical
magnetic resonance imaging (MRI) data from MRI-eligible participants of SA1. Using novel lesion-symptom
and functional-anomaly mapping methods, test hypotheses regarding associations between specific lesion
locations and deficits. Confirm that, in analogy to findings from aphasia research, stroke survivors with
visuospatial deficits show increased contralesional task-evoked activation, and that it relates to performance.
In addition to identifying the fundamental and dissociable components of visuospatial ability and their neural
basis, the results will allow us to (1) improve RH stroke diagnostics of by identifying tests that are highly
sensitive and specific to RH stroke, (2) provide more accurate outcome prognoses based on test results and
lesion characteristics, and (3) customize rehabilitation based a patient’s visuospatial profile. They will also lay
the basis for clinical trials evaluating noninvasive neurostimulation (rTMS, tDCS) for boosting rehabilitation of
visuospatial deficits by modulating contralesional brain activation.
