PubMed2005
BPD is often associated with cognitive deficits that tend to be present regardless of mood state. Greater impairments tend to be seen in BPD patients who are older, have an early onset of the disease, and suffer a more severe course of illness. The literature also suggests that cognitive deficits are present early in patients with BPD and may be cumulative, showing an association with the number of affective (particularly depressed) episodes over time. Cognitive deficits in BPD may share some common characteristics with those seen in patients with schizophrenia, although the latter tend to show much greater and generalized cognitive impairment. For example, unlike patients with schizophrenia, patients with BPD typically do not score lower than normal persons on measures of global intellectual ability. There also is not overwhelming evidence of laterality or localization of cognitive deficits in BPD, although debate in the literature continues. More visuospatial deficits tend to be found in BPD and UPD than in schizophrenia, thereby raising the possibility of greater involvement of right hemisphere systems in mood disorders. In general, despite variability across investigations, deficits in executive functioning, episodic memory,sustained concentration, and, to a lesser extent, visuospatial skills seem to be the most consistent areas of impairment in BPD. Just as neuroimaging anomalies have been well documented in schizophrenia, structural brain abnormalities have been noted in BPD,most commonly involving the basal ganglia or white matter. Specific comparisons of cerebral atrophy and ventricular size between patients with schizophrenia and BPD have not been definitive, making it difficult to draw conclusions about structural brain abnormalities that might be specific to BPD. Nonetheless, there is enough evidence to suggest that white-matter abnormalities are reported with a greater frequency in BPD patients than in patients with UPD or schizophrenia. Functional neuro-imaging studies of mood disorders have indicated that the frontal cortex,basal ganglia, and temporal lobes are involved. The relationships between neuroimaging and neurocognitive abnormalities in BPD are worthy of additional investigation. Clearly, efforts directed toward phenotyping neuropsychiatric disorders using such measures, in addition to other clinical, neuroimaging, neurophysiologic, and genotypic information, may yield important insights into the development, nature, and course of illness. It is hoped that this understanding will lead to better identification of individuals who may be prone to greater cognitive impairment or decline and those who might be more responsive to specific treatments.