Early Psychosis Study Links Brain Connectivity to Cognition
Psychosis is not just about what a person sees or hears. It’s also about what they can’t do. For individuals experiencing their first episode of psychosis, the struggle to focus, remember, or plan can be more debilitating than the hallucinations or delusions that often define the condition. Now, a new brain imaging study offers a potential biological explanation for these cognitive deficits.
The problem is profound. While antipsychotic medications can often manage so-called “positive” symptoms, they frequently fail to improve the cognitive fog that prevents patients from returning to school or work. Researchers at the University of Southern California’s Mark and Mary Stevens Neuroimaging and Informatics Institute have identified a specific pattern of brain miscommunication that appears directly linked to the severity of these cognitive issues, a finding published in the American Journal of Psychiatry.
The study suggests a fundamental imbalance in how the brain allocates its resources, with critical networks failing to properly engage and disengage.
This isn’t just theory. The USC team used functional magnetic resonance imaging (fMRI) to compare the brains of 131 patients with first-episode psychosis (FEP) against 132 healthy control subjects. The fMRI technology doesn’t take a static picture; instead, it tracks blood flow, a proxy for neural activity, to map how different brain regions communicate while a person is at rest.
Decoding the Brain’s Networks
Your brain has an internal chatter. Even when you’re doing nothing, distinct networks of neurons are firing in synchronized patterns. The study focused on two of the most important ones: the salience network (SN) and the default mode network (DMN).
Think of the salience network as the brain’s bouncer. It’s an attentional filter, constantly scanning your internal and external environment to decide what’s important enough to deserve your conscious focus. But the default mode network is what takes over when you’re mind-wandering or thinking about yourself. It’s the network for introspection and daydreaming.
In a healthy brain, these two networks operate like a seesaw. When one is active, the other is quiet. This dynamic allows you to shift focus from an external task to an internal thought and back again. The USC study, however, found this seesaw was broken in patients with early psychosis.
A Tale of Two Networks
The results were stark. The FEP patient group showed significant cognitive impairment across multiple domains when tested with the MATRICS Consensus Cognitive Battery, a standardized set of tests for cognition. The fMRI scans then provided a potential reason why.
Patients with psychosis displayed what scientists call hyperconnectivity—stronger-than-normal connections—between their salience network and other brain regions. Their attentional filter was seemingly stuck in overdrive. Simultaneously, these same patients showed hypoconnectivity, or weaker-than-normal connections, within their default mode network. Their capacity for orderly internal thought appeared diminished, according to the imaging data.
So, the two systems weren’t just out of sync; their dysregulation was directly tied to real-world problems. The researchers found a direct correlation: the more pronounced the hyperconnectivity of the salience network, the poorer the patient’s performance on tests of working memory and attention. This suggests the brain’s inability to quiet its “what’s important now?” filter directly interferes with its ability to hold and manipulate information.
Beyond Diagnosis: A Hunt for Biomarkers
This finding is more than an academic curiosity. It points toward a potential biomarker—an objective, measurable biological sign—for the cognitive symptoms of psychosis. A psychiatrist currently relies on patient interviews to gauge cognitive function. But an fMRI scan showing SN-DMN imbalance could one day provide a concrete metric of the problem and a way to measure if a treatment is working.
The road to the clinic, however, is long. Translating complex fMRI connectivity maps into a routine diagnostic tool won’t be simple. The compute power and analytical expertise required to process this kind of data aren’t available at most hospitals. And it’s crucial to remember that this study shows a correlation, not a definitive cause-and-effect relationship.
Still, the data provides a clear target. Instead of developing drugs that broadly dampen dopamine activity, pharmaceutical companies could investigate compounds that specifically modulate the activity of the salience or default mode networks. Non-invasive treatments like transcranial magnetic stimulation (TMS) could also, in theory, be deployed to try and rebalance the faulty connectivity.
The USC team is now planning to track these patients over several years. They want to determine if these initial connectivity patterns can predict an individual’s long-term clinical outcome or if the patterns change in response to treatment and time.
