Background: Aphasia may result from lesions to basal ganglia, thalamus, and capsular/pericapsular white-matter (i.e., subcortical structures). Lesions to these structures that produce language disturbances usually impair motor and/or sensory function(s), as well. Given the neurobehaviorally-salient networks to which these structures contribute, disturbances of executive function, comportment, emotional regulation, and/or motivation also should accompany subcortical aphasias. As this association is uncommonly described, we present a case of acute subcortical stroke producing nonfluent aphasia, apathy, and pathological laughing. Case History: A 53-year-old, right-handed woman with history of tobacco use and hyperlipidemia presented 3 days after sudden-onset of reduced spontaneous speech, impaired naming and word-finding, semantic paraphasias, and diminished self-care. Examination revealed reduced phrase lengths, brief, uncontrollable, stereotyped, and contextually inappropriate bursts of laughter, and diminished goal-directed thought, emotion, and behavior. The only elemental neurological abnormality was mild reflex asymmetry at the right triceps. Magnetic resonance imaging (MRI) revealed an acute 1.5-cm lesion involving the left genu and adjoining portions of the anterior and posterior limbs of the internal capsule, medial aspect of the globus pallidus, anterior, lateral, and ventral thalamic nuclei, and ventral striatum. Conclusions: The combination of anterior subcortical aphasia syndrome, apathy, and pathological laughing experienced by this patient are explained by an acute lesion involving subcortical gray and white matter structures at the point of intersection between language-related circuits, the anterior cingulate circuit, and descending corticobulbar tracts. Standard assessment methods did not readily identify the neurobehavioral features of this stroke, the clinical implications of which will be discussed.