Recent advancements in neuroimaging have provided compelling evidence supporting a longstanding hypothesis regarding the underlying mechanisms behind episodes of psychosis.
Talking about the theory, psychosis occurs through the disruption of the networks that regulates the skill of concentration. The disruption causes people to experience the things that are not true in the real world called hallucinations and sticking to unreal beliefs known as delusions. Though psychosis can be, and often is, linked to severe mental illnesses like schizophrenia, its symptoms can intensify or become less noticeable and can occur independently from an underlying mental health condition.
For many years scientists have been unable to unravel what sequences of psychosis in the brain make it function abnormally. A problem that is worth mentioning is that studies generally use patients who previously had the long-term treatment with antipsychotic drugs. This hinders recognition of whether the brain changes are directly attributed to the condition itself or indirectly to the undesirable effects of the medication.
Last week a large-scale brain-scan investigation (published in Molecular Psychiatry on the 11th of April) was conducted and its main aim was to shed light on the initial processes (starting in early life) that develop psychosis. This program is designed to ensure timely detection and the most appropriate therapeutic intervention.
“It not only takes place in adulthood, but the irregularities start as early as age 7 or 8,” quoted Kaustubh Supekar, lead author of the study and clinical associate professor in psychiatry and behavioral sciences at Stanford University School of Medicine.
In order to find the likes of these patients, the study focused on people between the ages of 6 and 39 who had psychosis and a genetic disorder known as 22q11.2 deletion syndrome. This syndrome is as a consequence from the physiological absence of a chromosome 22 piece. Loved ones of people with this syndrome might have other health risks also associated with them, such as heart problems, attention-deficit/hyperactivity disorder (ADHD), and autism. However, this syndrome average 30% of possibility of development of psychosis, schizophrenia, or both.
The team scanned a brain with fMRI in seeking changes in blood flow that have a direct relation to the neuronal activity. The study was conducted on 878 subjects, which involved 101 individuals who had 22q11.2 del Syndrome, with some of them diagnosed with psychosis and some without the condition. To add on to this, 120 individuals were also recruited all with “psychosis of unknown origin.”
Adams went on saying that the study was uncommon in that it had considered individuals who had not experienced psychosis in addition to those with ADHD and autism that seldomly received consideration in classification studies. He suggested this very characteristic highlighted the uniqueness of the found brain signatures that differentiated psychosis from other neurological disorders.
Brain scans in patients with disorders of psychosis showed unique patterns that were not seen in the control groups. Such patterns were noticeable in these two core elements of the brain’s “salience network.” This network is responsible for steering our attention toward either inner thoughts or outer stimuli and thus, prioritizing what is relevant and actual. Notably, the scans highlighted the significance of two nodes within this network: the anterior insula, which acts as a filter of sifting out irrelevant information, and the ventral striatum area, which guesses about which information has a greater worth to us.
The researchers aim to concentrate on those crucial brain regions using established techniques such as brain stimulation, trying to assess if it could help to stop or at least delay the outbreak of psychosis in the risky individuals. In addition, they try to evaluate these drugs on the specific elements of the salience network, which will clear the mechanism of action more deeply.
