Psychosis after ketamine: What happens in the brain? - Medical News Today
- Researchers investigated whether ketamine may induce changes in the brain that are similar to psychosis.
- They found that ketamine increases background noise, which may interfere with how the brain processes sensory signals.
- The researchers conducted their study on rats, meaning that further research is needed to see how the findings may apply to humans.
Schizophrenia is characterized by changes in how a person perceives reality, including experiencing persistent delusions, hallucinations, and disorganized thinking. The condition affects around
The exact cause of schizophrenia remains unknown. However, studies suggest that the condition may arise from environmental, psychological, and genetic factors.
A drug known as ketamine induces a mental state similar to psychosis in healthy individuals by
Experts believe that similar changes in NMDA receptors could be linked to perception changes in schizophrenia. How this may be the case, however, has remained unknown.
Recently, researchers examined how ketamine affects sensory perception in the brains of rats.
They found that ketamine increased "background noise" in the brain, making sensory signals less defined or pronounced. This, they noted, may explain the distorted perception of reality among people with schizophrenia or psychosis.
Their findings appeared in the
Dr. Sam Zand, DO, the chief medical officer for Better U who was not involved in the study, commented on these findings, telling Medical News Today that they "suggest that dysfunction in NMDA receptors may play a role in the development of psychosis."
"The study provides new insights into the mechanism by which ketamine may induce psychotic symptoms. The findings may help to inform the development of new treatments for psychosis that target NMDA receptors or brain noise," he added.
For the study, the researchers looked at the effects of ketamine on sensory perception in seven male lab rats. To do so, they first implanted rats with electrodes to record electrical activity in their brains.
They then simulated their whiskers and recorded the brain's responses before and after ketamine.
More specifically, the researchers monitored how ketamine affects beta and gamma oscillations in a neural network that transmits signals from sensory organs to the brain.
Beta oscillations are brainwaves that range from 17–29 Herz (Hz), while gamma waves range from 30–80 Hz. The frequencies are crucial for processing sensory information.
In the end, the researchers found that ketamine increased power in both beta and gamma oscillations even before they stimulated the rats' whiskers.
They also found, however, that post-stimulus and after ketamine administration, the amplitude of the rats' beta and gamma oscillations decreased, which is linked to impaired perception.
They further noted that ketamine increased noise in gamma frequencies, which is also linked to an impaired ability to process sensory signals.
The researchers suggested that their findings mean that the distorted reality experienced in psychosis and schizophrenia may be triggered by more background noise, which in itself may be caused by malfunctioning NMDA receptors causing an imbalance of inhibition and excitation in the brain.
"The discovered alterations in thalamic and cortical electrical activity associated with ketamine-induced sensory information processing disorders could serve as biomarkers for testing antipsychotic drugs or predicting the course of disease in patients with psychotic spectrum disorders," says Dr. Sofya Kulikova, senior research fellow at the HSE University in Perm, Russia, one of the study authors.
MNT spoke with Dr. Howard Pratt, psychiatrist and behavioral health medical director at Community Health of South Florida, not involved in the study, about its limitations. He emphasized that:
"The limitations of these findings are really that while we have clear correlation, we don't yet have causation. Conditions like psychosis have numerous causes, which could be, for example, elevations in dopamine, which is the target of treatment with people carrying a diagnosis of schizophrenia. I look forward to seeing what happens when the research goes beyond animal studies."
We also spoke with Dr. James Giordano, Pellegrino Center professor of neurology and biochemistry at Georgetown University Medical Center, not involved in the study, about the study's limitations.
"A major limitation of the study is that it only investigated ketamine-induced effects, and thus, while useful and viable for gaining insights to ketamine's activity in a rat model, may not provide direct translation to understand non–drug–induced dissociative, and psychotic states in humans," he cautioned.
"It may be, for example, that the effects produced by ketamine in humans, while certainly being dissociative, and having certain characteristics of psychosis, are not completely representative or identical to the neurological mechanisms involved in other types of psychosis and schizophreniform disorders," Dr. Giordano further noted.
When asked about the study's implications, Dr. Giordano explained that "[t]hese findings are useful in that demonstration of ketamine's actions at defined brain networks may enable better understanding — and improved clinical applications — of its effects in humans."
"Additionally, by illustrating the roles of these brain nodes and networks involved in mediating dissociative states, we may develop improved insights — and possible treatments for — certain types of drug-induced psychoses, and perhaps other psychotic conditions, such as forms of schizophrenia, as well," he concluded.
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