There are a plethora of cognitive sequelae in addition to neglect and extinction that arise with unilateral right hemispheric stroke (RHS). Cognitive deficits following non-dominant (right) hemisphere stroke are common with unilateral neglect and extinction being the most recognized examples. The severity of RHS is usually underestimated by the National Institutes of Health Stroke Scale (NIHSS), which in terms of lateralized right hemisphere cognitive deficits, tests only for visual inattention/extinction. They account for 2 out of 42 total possible points. Additional neuropsychiatric sequelae include but are not limited to deficiencies in affective prosody comprehension and production (aprosodias), understanding and expressing facial emotions, empathy, recognition of familiar faces, anxiety, mania, apathy, and psychosis. These sequelae have a profound impact on patients' quality of life; affecting communication, interpersonal relationships, and the ability to fulfill social roles. They also pose additional challenges to recovery. There is presently a gap in the literature regarding a cohesive overview of the significant cognitive sequelae following RHS. This paper serves as a narrative survey of the current understanding of the subject, with particular emphasis on neuropsychiatric poststroke syndromes not predominantly associated with left hemisphere lesions (LHL), bilateral lesions, hemiplegia, or paralysis. A more comprehensive understanding of the neuropsychological consequences of RHS extending beyond the typical associations of unilateral neglect and extinction may have important implications for clinical practice, including the ways in which clinicians approach diagnostics, treatment, and rehabilitation.

Recognition of faces of family members, friends, and colleagues is an important skill essential for everyday life. Individuals affected by prosopagnosia (face blindness) have difficulty recognizing familiar individuals. The prevalence of prosopagnosia has been estimated to be as high as 3%. Prosopagnosia can severely impact the quality of life of those affected, and it has been suggested to co-occur with conditions such as depression and anxiety.

To determine real-world diagnostic frequency of prosopagnosia and the spectrum of its comorbidities, we utilized a large database of more than 7.5 million de-identified electronic health records (EHRs) from patients who received care at major academic health centers and Federally Qualified Health Centers in New York City. We designed a computable phenotype to search the database for diagnosed cases of prosopagnosia, revealing a total of n = 902 cases. In addition, data from a randomly sampled matched control population (n = 100,973) were drawn from the database for comparative analyses to study the condition's comorbidity landscape. Diagnostic frequency of prosopagnosia, epidemiological characteristics, and comorbidity landscape were assessed.

We observed prosopagnosia diagnoses at a rate of 0.012% (12 per 100,000 individuals). We discovered elevated frequency of prosopagnosia diagnosis for individuals who carried certain comorbid conditions, such as personality disorder, depression, epilepsy, and anxiety. Moreover, prosopagnosia diagnoses increased with the number of comorbid conditions.

Results from this study show a wide range of comorbidities and suggest that prosopagnosia is vastly underdiagnosed. Findings imply important clinical consequences for the diagnosis and management of prosopagnosia as well as its comorbid conditions.

This investigation examined whether impairment in configural processing could explain deficits in face emotion recognition in people with Parkinson's disease (PD). Stimuli from the Radboud Faces Database were used to compare recognition of four negative emotion expressions by older adults with PD (n = 16) and matched controls (n = 17). Participants were tasked with categorizing emotional expressions from upright and inverted whole faces and facial composites; it is difficult to derive configural information from these two types of stimuli so featural processing should play a larger than usual role in accurate recognition of emotional expressions. We found that the PD group were impaired relative to controls in recognizing anger, disgust and fearful expressions in upright faces. Then, consistent with a configural processing deficit, participants with PD showed no composite effect when attempting to identify facial expressions of anger, disgust and fear. A face inversion effect, however, was observed in the performance of all participants in both the whole faces and facial composites tasks. These findings can be explained in terms of a configural processing deficit if it is assumed that the disruption caused by facial composites was specific to configural processing, whereas inversion reduced performance by making it difficult to derive both featural and configural information from faces.

Visual deficits following stroke are frequently subtle and are often overlooked. Even though these visual deficits may be less overt in nature, they are still debilitating to survivors. Visual deficits have been shown to negatively impact cognition, mobility, and activities of daily living (ADL). There is little consistency across healthcare facilities regarding protocol for assessing vision following stroke.

This research was designed to describe a profile for patients exhibiting visual deficits following stroke, examine the role of occupational therapists in vision assessment, and discuss a potential model to provide a protocol for collaboration with an eye care professional as part of the rehabilitation team.

The sample consisted of 131 patients in an inpatient rehabilitation (IPR) unit who were identified as having potential visual deficits. Occupational therapists on an IPR unit administered initial vision screenings and these patients were subsequently evaluated by the consulting optometrist. Frequencies were calculated for the appearance of functional symptoms, diagnoses, and recommendations. Correlations were also computed relating diagnoses and recommendations made.

All patients referred by the occupational therapist for optometrist evaluation had at least one visual diagnosis. The most frequent visual diagnoses included: saccades (77.7%), pursuits (61.8%), and convergence (63.4%). There was also a positive correlation between number of functional symptoms seen by occupational therapists and visual diagnoses made by the optometrist (r  =  0.209, P  =  0.016).

Results of this study support the need for vision assessment following stroke in IPR, confirm the role of occupational therapists in vision assessment, and support the need for an optometrist as a member of the rehabilitation team.

Ischemic stroke results in diverse pathophysiologies, including cerebral inflammation, neuronal loss, cognitive dysfunction, and depression. Studies aimed at identifying therapeutic solutions to alleviate these outcomes are important due to the increase in the number of stroke patients annually. Recently, many studies have reported that orexin, commonly known as a neuropeptide regulator of sleep/wakefulness and appetite, is associated with neuronal cell apoptosis, memory function, and depressive symptoms. Here, we briefly summarize recent studies regarding the role and future perspectives of orexin in post-ischemic stroke. This review advances our understanding of the role of orexin in post-stroke pathologies, focusing on its possible function as a therapeutic regulator in the post-ischemic brain. Ultimately, we suggest the clinical potential of orexin to regulate post-stroke pathologies.

This study describes the case of CH, a 68-year-old left-handed woman who suffered a right temporo-parieto-occipital infarct in the territory of the middle cerebral artery and who exhibits severe proper name anomia. During the acute stage, CH was diagnosed with severe amnestic aphasia (Aachen Aphasia Test). Her lesion mirrors those of left hemisphere impairing the processing proper names, without an aphasic language disorder in general. Seven weeks later, language improved to a mild amnestic aphasia that currently does not interfere with her daily life. However, the use of proper names in both the visual and auditory modalities was still impaired and showed no improvement after 6 months of speech therapy. While not being able to name family members or familiar persons, she was, however, still able to describe the persons' backgrounds along with some additional semantic information. Furthermore, in a simple semantic design test, CH was selectively impaired in correctly classifying proper names into their respective word classes. Conversely, she was able to correctly name and classify other word categories (e.g., common nouns). In the subsequent study, we assessed the modalities "auditory comprehension," "picture naming," and "reading comprehension" and classified her responses in the categories "correctly named," "correctly classified," "correctly described attributes" (e.g., occupation) and "falsely named." The results were compared with those of an age-matched healthy control group. In the visual task, CH correctly named 80% of the visualized objects, 3% of the familiar persons and 15% of the familiar city views.

Patients with Capgras syndrome (CS) adopt the delusional belief that persons well-known to them have been replaced by an imposter. Several current theoretical models of CS attribute such misidentification problems to deficits in covert recognition processes related to the generation of appropriate affective autonomic signals. These models assume intact overt recognition processes for the imposter and, more broadly, for other individuals. As such, it has been suggested that CS could reflect the "mirror-image" of prosopagnosia. The purpose of the current study was to determine whether overt person recognition abilities are indeed always spared in CS. Furthermore, we examined whether CS might be associated with any impairments in overt affective judgments of facial expressions. We pursued these goals by studying a patient with Dementia with Lewy bodies (DLB) who showed clear signs of CS, and by comparing him to another patient with DLB who did not experience CS, as well as to a group of healthy control participants. Clinical magnetic resonance imaging scans revealed medial prefrontal cortex (mPFC) atrophy that appeared to be uniquely associated with the presence CS. We assessed overt person recognition with three fame recognition tasks, using faces, voices, and names as cues. We also included measures of confidence and probed pertinent semantic knowledge. In addition, participants rated the intensity of fearful facial expressions. We found that CS was associated with overt person recognition deficits when probed with faces and voices, but not with names. Critically, these deficits were not present in the DLB patient without CS. In addition, CS was associated with impairments in overt judgments of affect intensity. Taken together, our findings cast doubt on the traditional view that CS is the mirror-image of prosopagnosia and that it spares overt recognition abilities. These findings can still be accommodated by models of CS that emphasize deficits in autonomic responding, to the extent that the potential role of interoceptive awareness in overt judgments is taken into account.