tDCS is showing promise: “…improved such that [schizophrenia] patients were indistinguishable from healthy control subjects”…
Executive control and flexible adjustment of behavior following errors are essential to adaptive functioning. Loss of adaptive control may be a biomarker of a wide range of neuropsychiatric disorders, particularly in the schizophrenia spectrum. Here, we provide support for the view that oscillatory activity in the frontal cortex underlies adaptive adjustments in cognitive processing following errors. Compared with healthy subjects, patients with schizophrenia exhibited low frequency oscillations with abnormal temporal structure and an absence of synchrony over medial-frontal and lateral-prefrontal cortex following errors. To demonstrate that these abnormal oscillations were the origin of the impaired adaptive control in patients with schizophrenia, we applied noninvasive dc electrical stimulation over the medial-frontal cortex. This noninvasive stimulation descrambled the phase of the low-frequency neural oscillations that synchronize activity across cortical regions. Following stimulation, the behavioral index of adaptive control was improved such that patients were indistinguishable from healthy control subjects. These results provide unique causal evidence for theories of executive control and cortical dysconnectivity in schizophrenia.
“The ability to exert control over our behavior is fundamental to human cognition, and is impaired in many neuropsychiatric disorders. Here, we show evidence for the neural mechanisms of adaptive control that distinguish healthy people from people who have schizophrenia. We found that the noninvasive electrical stimulation phase aligns low-frequency brain rhythms and enhances functional connectivity. This brain stimulation modulated the temporal structure of low-frequency oscillations and synchrony, improving adaptive control. Moreover, we found that causal changes in the low-frequency oscillations improved behavioral responses to errors and long-range connectivity at the single-trial level. These results implicate theories of executive control and cortical dysconnectivity, and point to the possible development of nonpharmacological treatment alternatives for neuropsychiatric conditions.”
“The present study has important implications for translating these findings from the laboratory into the real world. The treatment of cognitive deficits has traditionally been the domain of pharmacology; however, there are several encouraging signs that transcranial electrical stimulation may offer a safe alternative or adjunct approach. For patients with schizophrenia, atypical antipsychotic drugs (e.g., clozapine, risperidone, olanzapine) can ameliorate some aspects of cognitive deficits. However, there are adverse side effects, such as obesity and diabetes, and some patients develop resistance. Therefore, there is a dire need for effective and noninvasive treatment options without the side effects. Over the past decade, tDCS has come into the spotlight, showing some promise as a drug-free intervention for neuropsychiatric illnesses, such as schizophrenia. Compelling rationales for using tDCS in schizophrenia include the fact that NMDA receptor dysfunction is implicated in schizophrenia pathophysiology and NMDA antagonists abolish tDCS effects, whereas NMDA agonists enhance tDCS effects. Second, schizophrenia is associated with deficits in neuroplasticity, specifically brain-derived neurotropic factor (BDNF)-dependent synaptic plasticity, and research has shown that dc stimulation promotes BDNF-dependent plasticity. Third, compared with other noninvasive stimulation methods, such as transcranial magnetic stimulation (TMS), tDCS is cost-effective, easy to use, portable, and safe, making this technique an attractive candidate as a supplementary neurointervention for people with severe neuropsychiatric conditions such as schizophrenia, which places a heavy personal and societal burden, reportedly costing more than $62.7 billion per year in the United States.”
“In summary, our findings demonstrate that the posterror slowing deficit of adaptive control in schizophrenia is governed, in part, by dysfunctional processes indexed by theta-band phase dynamics, which are abnormally decoupled from frontolateral oscillations important for the implementation of cognitive control. However, by stimulating medial-frontal cortex, considered by many to represent a fulcrum for the action-monitoring network, we were able to improve the behavioral and neural signatures of adaptive control in schizophrenia temporarily.”