Psychosis is a condition that causes a disconnect from reality. The main symptoms are hallucinations, delusions, disorganized thinking and behavior. Psychosis can be caused by mental health conditions like schizophrenia, bipolar disorder, or drug use. It can be a very distressing experience and lead to functioning difficulties. A common question is whether experiencing psychosis causes any permanent damage or changes to the brain. Here is an overview of what research shows regarding the potential lasting impacts of psychosis.
What happens in the brain during psychosis?
Psychosis involves profound changes in brain functioning. When experiencing psychosis, several important brain networks become disrupted:
- Dopamine system – Dopamine is a neurotransmitter involved in motivation, pleasure, and reward. Too much dopamine activity, especially in the striatum region, is linked to positive symptoms like delusions and hallucinations.
- Prefrontal cortex – This region is involved in executive functioning like planning and decision making. Impaired prefrontal cortex functioning contributes to disorganized thoughts and behavior.
- Hippocampus – The hippocampus is vital for memory formation and retrieval. Its disruption leads to memory problems.
- Default mode network – This network is active during internal thoughts and daydreaming. Its impairment can trigger thought disorganization.
- Salience network – This network determines what stimuli deserve attention. Its dysregulation causes delusions and hallucinations.
Brain imaging scans show that these networks are working abnormally during acute psychosis episodes. Next, we’ll see whether these changes can become permanent.
Grey matter loss
Several studies find that people who experience psychosis show reduced grey matter volume and thinner cortex layers compared to healthy individuals. Grey matter loss is detected in areas like:
- Prefrontal and temporal cortex
- Hippocampus
- Anterior cingulate
This gray matter reduction is seen in both first-episode psychosis patients and those with chronic schizophrenia. However, people in their first psychotic episode show less shrinkage. This suggests illness progression and repeated psychotic episodes may worsen the grey matter loss over time.
What causes the grey matter loss?
There are a few theories on what leads to the grey matter deficits:
- Toxic effects of psychosis – The chemical imbalances and overactive dopamine during psychosis may damage and kill brain cells.
- Medications – Antipsychotic drugs change brain volume, so medication effects likely contribute.
- Illness progression – More psychotic episodes over time may progressively impair the brain.
- Substance abuse – Heavy drug and alcohol use can independently shrink grey matter.
Is the loss reversible?
Unfortunately, research indicates the grey matter reductions do not completely reverse, even with successful treatment. However, early effective treatment may slow the progression. Some studies show medication can temporarily increase grey matter volume.
Cognitive deficits
In addition to structural changes, psychosis is linked to cognitive impairments that persist after the acute symptoms resolve. The deficits are most prominent in these areas:
- Processing speed
- Working memory
- Verbal learning and memory
- Attention
- Executive functioning
Cognitive problems are detected in first-episode psychosis patients and remain stable or worse over time. The deficits exist on a spectrum, with more severe dysfunction in schizophrenia than affective psychoses like bipolar disorder.
Do cognitive deficits improve?
Most patients do not return to premorbid cognitive functioning after the initial psychotic break. However, some cognitive recovery occurs in the first year, especially in processing speed, verbal memory, and executive functioning. Ongoing improvements are limited without effective treatment and cognitive remediation therapy.
Brain connectivity impairments
Psychosis disrupts normal communication between brain networks. While acute psychosis shows the most extensive connectivity abnormalities, some impairments persist after remission:
- Reduced connectivity within and between resting state networks like default mode, salience, and central executive networks
- Altered connectivity between prefrontal cortex, temporal lobes, thalamus, and cerebellum
This suggests functional communication disruptions between brain regions may not fully normalize between psychotic episodes. Persistent network impairments likely underlie the cognitive deficits in psychotic disorders.
Neurochemical changes
Psychosis induces alterations in neurotransmitters like dopamine, GABA, and glutamate. Studies indicate some neurotransmitter abnormalities persist after remission:
- Elevated presynaptic dopamine synthesis and release capacity in striatum
- Reduced GABA interneurons in prefrontal cortex
- Abnormal glutamate levels in thalamus
Ongoing dopamine dysfunction may explain why delusions and hallucinations recur in psychotic disorders. The neurochemical changes may also contribute to persistent cognitive impairments.
Brain aging
Emerging research indicates psychosis is associated with accelerated aging. Studies reveal people with schizophrenia show brain changes similar to healthy individuals who are decades older:
- Thinner cortex and prefrontal grey matter loss akin to 7-12 years of added aging
- Ventricular enlargement comparable to 5 years of extra aging
- Hippocampal volume reduction equivalent to 4-6 years of excess aging
- Greater cortical age-related thinning compared to peers
The aging gap is significant by the first psychotic episode and widens with recurrent episodes. Precise mechanisms are uncertain but likely involve stress, inflammation, neurotransmitter imbalance, medication effects, and circuit damage from psychosis.
Inflammation and oxidative stress
Research shows elevated inflammation and oxidative stress in the brains of psychosis patients, even in early-stage illness. Pro-inflammatory cytokines and oxidative stress markers remain elevated despite symptom improvement. Chronic inflammation and oxidative damage may contribute to ongoing brain changes in psychotic disorders.
Neuroanatomical differences
Cross-sectional neuroimaging studies reveal subtle anatomical brain differences in people vulnerable to psychosis before they become ill. These include:
- Enlarged ventricles
- Reduced temporal and prefrontal lobe volume
- Thalamus and hippocampus abnormalities
The abnormalities are most prominent in people who later develop schizophrenia. This suggests neurodevelopmental and genetic factors make some brains more vulnerable to psychosis-induced damage.
Neuroprogression
The cumulative evidence shows psychosis and schizophrenia are associated with neuroprogressive brain changes that evolve over time. This neuroprogression process includes:
- Ongoing loss of gray matter in frontal, temporal, and limbic regions
- Deterioration of executive functioning
- Worsening processing speed, memory, and social cognition
- Shrinking brain volume and enlarged ventricles
- Accelerated aging of the brain
Repeated acute episodes seem to drive much of the neurodegeneration.
Does medication help?
Research on whether antipsychotic medications can prevent brain changes is mixed:
- Typical antipsychotics like haloperidol show limited effects on grey matter loss.
- Atypical antipsychotics may temporarily increase grey matter volume but effects are small and transient.
- Some studies find no neuroprotective differences between antipsychotic classes.
- Treating earlier in psychosis and continuously may provide more brain benefits.
Overall, medications reduce symptoms but do not seem to markedly slow progressive brain changes in most patients. However, treatment is still vital for functional recovery.
Can cognitive training help?
Cognitive remediation training, especially when combined with psychiatric rehabilitation, can lead to modest improvements in cognition and daily functioning. Benefits may include:
- Improved processing speed, memory, attention, executive functioning
- Increased prefrontal and temporal grey matter volume
- Lasting changes in brain activity
Cognitive training likely works by strengthening new neural pathways and bypassing damaged circuits. It needs to be ongoing for sustained effects.
Are the effects reversible?
The brain changes with psychosis appear only partially reversible. Research shows:
- Grey matter loss does not completely reverse after psychosis treatment.
- Cognitive deficits remain stable or improve slightly with treatment.
- Some connectivity impairments may normalize between episodes.
- Brain aging effects persist and likely worsen with repeated episodes.
- Early, continuous treatment may limit damage by reducing psychosis frequency and severity.
- Cognitive remediation therapy can strengthen new neural pathways.
While not fully reversible, early intervention and maintenance treatment are vital for limiting progressive deterioration and improving long-term outcomes.
Are the effects permanent?
There is strong evidence that psychosis causes lasting structural, functional, and cognitive changes to the brain. These effects are detectable after a first psychotic episode and worsen with repeated acute episodes. Findings suggest:
- Grey matter deficits remain stable or progress after the first break.
- Cognitive deficits continue even after psychosis remits.
- Some connectivity impairments persist between psychotic episodes.
- Accelerated aging processes continue over the illness course.
So while not completely irreversible, the brain impacts of psychosis appear to be chronic and enduring in many patients. Early treatment is critical to limit permanent effects.
Conclusion
Experiencing psychosis has profound effects on the brain that do not fully resolve. Grey matter loss, cognitive deficits, accelerated aging, and neural connectivity changes persist after an initial psychotic episode. These brain changes are exacerbated with repeated unmedicated psychotic breaks. The evidence indicates psychosis causes long-term, potentially permanent brain changes in many patients. However, research also shows early intervention and maintenance treatment after a first break can limit damage from psychosis. Cognitive rehabilitation therapies also help strengthen new neural pathways. So while not completely reversible, prompt treatment and lifestyle changes can improve outcomes and reduce permanent brain changes from psychosis.