Neurocognitive deficits are core features of schizophrenia that may determine functional outcome. Working memory (WM) deficit has been identified as one of the most important components of the neurocognitive deficits in schizophrenia. WM is a limited-capacity, active short-term memory system that guides and controls behavior. A majority of patients with schizophrenia and about half of their healthy first-degree relatives have WM deficits and these deficits are linked to poor social and adaptive functioning yet the origins and consequences of WM deficit are unclear. Thus it has not been possible to develop targeted interventions that might ameliorate WM deficits and improve adaptive functioning.
We are interested in to identifying mechanisms that are central to WM deficit and their neural correlates. We also want to examine the effects of WM deficit on social functioning. Cognitive and neuroanatomical data suggest that selective attention and affect modulate encoding and maintenance in WM but schizophrenic patients are unable to effectively integrate attention and affect to guide goal-directed behavior.
- We investigate the roles of perceptual, attentional and affective factors in encoding to specify both optimal and detrimental encoding conditions. Encoding affects all forms of memory and thus has far-reaching consequences. In addition to impaired encoding there is good evidence for abnormal maintenance in schizophrenia.
- The effects of attentional control and affect on maintenance are examined to identify where vulnerabilities lie. We are particularly interested in studying the role mental imagery in the manipulation of memory representations. A series of experiments on manipulation and maintenance interactions are currently being conducted.
- The roles of prefrontal and parietal cortices in normal and abnormal WM are being investigated with event-related fMRI and near infrared optical imaging experiments. The neural correlates of correct and incorrect performance are observed to elucidate the difference between remembering and forgetting in the brain.
To summarize, we aim to identify the key components of WM deficits in schizophrenia. We recruit unaffected siblings of schizophrenic patients to observe potential deficits as well as spared abilities. We also study bipolar individuals to compare the two psychotic disorders. Identification and elucidation of core neurocognitive deficits of schizophrenia will contribute towards the understanding of the complex interplay between cortical functions and cognitive deficits in schizophrenia. Moreover, specifying abnormal mechanisms within WM in relation to attention, affect and brain activation patterns could lead to targeted strategies that might ameliorate WM deficits and improve adaptive functioning in schizophrenia.
Parkinson's Disease results in a wide range of motor, cognitive and affective deficits. With Dr. Joseph Neimat in Neurosurgery, we are investigating working memory deficits in Parkinson's disease patients who have deep brain stimulation (DBS) device implanted to stimulate the subthalamic nucleus. DBS is a relatively new treatment option when drugs no longer work. When DBS is switched on, there is a remarkable improvement in motor behavior. Although the efficacy of DBS for movement initiation and control is excellent, there is some evidence to suggest that cognitive functioning may get worse. We are examining working memory on and off DBS in Parkinsonian patients. In addition, we collect near infrared optical imaging data during a spatial working memory task in Parkinson's disease patients to examine frontal cortical activity in relation to DBS stimulation in the subthalamic nucleus.