Poststroke subcortical aphasia and neurobehavioral disturbances without motor or sensory deficits.

To the Editor: Subcortical aphasia may result from lesions of the basal ganglia, anterolateral nuclei of the thalamus, and capsular/pericapsular whitematter of the language-dominant hemisphere. Subcortical aphasia associated with lesions of the posterior limb of the internal capsule (ICp) and adjacent subcortical structures typically involves impaired picture naming (letters better than objects), rapid fluent speechwith paraphasias and extended jargon, poor comprehension, and impaired repetition. Contralateral disturbances of elementary motor and sensory function typically occur; with posterior extension of the capsular lesion, these disturbances may be accompanied by visual field deficits and auditory dysfunction. Subcortical aphasia associated with lesions of the anterior limb of the internal capsule (ICa) and adjacent structures (often including the genu of the internal capsule [ICg]) typically involves impaired picture naming (objects better than letters), grammatical but slow dysarthric speech output, good semantic comprehension with impaired syntactic comprehension, and repetition impairments primarily for low-probability sentences (with articulatory distortions and word omissions); impaired articulatory agility, buccofacial apraxia, and contralateral hemiparesis also are typically present. Subcortical aphasia associated with lesions involving the ICa, ICp, and adjacent subcortical structures features more severe language disturbances (i.e., global aphasia) and contralateral motor, sensory, and visual field deficits. The neuropsychiatric, motor, and sensory concomitants of subcortical aphasia follow capsular anatomy (Figure 1 [A]). The frontopontine, thalamofrontal, and thalamostriate fibers in the ICa subserve circuits regulating emotion, comportment, motivation, and executive function. The ICg comprises fibers of the corticonuclear tract, connecting the motor cortex to contralateral cranial nerve nuclei. The ICp comprises fibers of the corticospinal (pyramidal or voluntary motor) tract, as well as sensory fibers originating from the thalamus and, to a lesser extent, from the medial lemniscus; the distal one-third of the ICp includes fibers of the optic and acoustic radiations, as well as temporopontine, parietopontine, and occipitopontine fibers. Concomitant neuropsychiatric disturbances (especially executive dysfunction, disordered comportment, diminished motivation, and/or emotional dysregulation) would be expected among persons with subcortical aphasia involving lesions of the ICa and adjacent subcortical structures. By contrast, elementary motor impairments are expected concomitants of subcortical aphasia associated with lesions involving the ICg and/or ICp, and sensory impairments are expected accompaniments of lesions involving the ICp. Contrary to these expectations, we present a case of acute subcortical stroke involving the ICg and ICp as well as adjacent subcortical structures (with caudal extension) associated with subcortical aphasia, apathy, and pathological laughing and no motor or sensory deficits.