Article on Translating Symptoms to Neurobiological Targets

Integrated findings on the early symptomatic course of schizophrenia and in vivo evidence of brain aberrations.
BSs viewed as subtle, subclinical disturbances in mental processes, expressing the underlying neurobiological abnormalities.
Other symptoms like delusions and hallucinations considered secondary, resulting from dysfunctional beliefs and coping styles related to BSs.

Can occur in various mental disorders, particularly affective disorders.
A subset of cognitive and perceptual BSs specific to psychosis is used in risk criteria for psychosis.
Recognized for early detection of psychosis, yet neurobiological research linking BSs to brain function is still emerging.

Basic symptoms are self-experienced disturbances in:
- Stress tolerance
- Drive
- Affect
- Thinking
- Speech
- Body perception
- Motor action
- Central-vegetative functions.
Experienced with full insight, rendering them distinct from observable negative symptoms and positive symptoms, which are seen as normal by the individual.
Integral to psychosis and appear at various disorder stages, conceptualized as “self-disorders” in combination with selected attenuated psychotic symptoms (APS).

Huber’s studies linked BSs to brain function through observable abnormalities in areas like the basal ganglia and limbic system, suggesting BSs reflect direct symptomatic expressions of cerebral dysfunction.
Abnormal EEG rhythms were hypothesized as transient and only present in early psychotic stages.

Research indicates that although most BSs are not solely specific to psychosis, certain BSs are critical for developing first-episode schizophrenia. 14 BSs identified as indicative.
A meta-analysis reported conversion rates of up to 54.9% within 4 years in COGDIS samples, significantly higher than those meeting UHR criteria.
COGDIS remains one of the three recommended criteria for CHR assessment by the European Psychiatric Association.

Neurocognitive deficits are prevalent in schizophrenia, also observable in CHR samples.
Studies suggested inconsistent findings concerning BS samples mainly affecting executive control and verbal memory.
Patients qualifying solely under BS criteria showed fewer cognitive deficits than those with APS or brief limited intermittent psychotic symptoms (BLIPS). This indicates a potential precedence of BSs over neurocognitive impairments.

Neurochemical findings highlight roles for various neurotransmitters (dopaminergic, glutamatergic, serotonergic, GABAergic) in schizophrenia.
Current studies focused on dopamine, glutamate, and GABA, revealing significant evidence for presynaptic dopamine synthesis increase in APS patients, although research on BS samples is needed.

Ketamine and endocannabinoid systems have been linked with BSs, suggesting that cannabis and ketamine use may relate to cognitive and perceptive BSs.
Cannabis-using CHR patients exhibit more BSs than non-users.

EEG and magnetoencephalographic studies reveal significant changes in neural activity correlating with BS manifestations.
Event-related potentials showed reduced emotion recognition abilities in CHR groups, along with indications of disturbances in information processing across neurocognitive measures.

Overview of various neurobiological studies exploring potential relationships between basic symptoms, neurocognitive function, and disease vulnerability.
Notable correlations between BSs, neurocognitive functioning, and structural/functional abnormalities in brain regions indicative of psychosis.

Five MRI studies show relationships between BSs and morphological changes in brain structures, focusing on groups with different risk levels for psychosis.
Findings indicate gray matter reductions in specific cortices among individuals with BSs.

fMRI studies examining BSs show altered activation patterns in first-episode schizophrenia patients, revealing significant associations between BS severity and connectivity within brain regions related to self-other distinctions.

Emphasizes the need for further exploration into neurobiological origins of BSs to create effective early detection tools and interventions for psychosis.
Highlights the importance of understanding BSs as potential early indicators of psychosis and their implications for therapeutic approaches.

Basic symptoms reflect subtle and heterogeneous manifestations of neurobiological abnormalities in schizophrenia.
The CHR paradigm shows promise in linking subjective cognitive alterations and neurobiological dysfunctions, essential for improving diagnosis and treatment strategies for psychosis.