Accumulation of risk factors and transition to psychosis: clinical case of a high-risk individual

Brief Introduction: The first episode psychosis (FEP) often results from the interaction between individual vulnerability and environmental factors. The early identification of high-risk and ultra-high-risk mental states continues to represent a significant clinical challenge.

Aims

To describe a case of FEP in an individual with multiple cumulative risk factors, discussing the relative contribution of genetic, neurobiological, and environmental factors, as well as the challenges inherent to differential diagnosis and implications for clinical practice.

Methods

A 50-year-old man, single, unemployed, with a history of recurrent depressive disorder and long-standing substance use disorder, under psychiatric follow-up. No prior history of psychotic symptoms. Relevant medical history includes an anterior communicating artery aneurysm, surgically corrected 5 years earlier. Family history of bipolar disorder (father and sister).

The patient was enrolled in a methadone substitution program, with regular cocaine use initiated approximately 3 years prior. He had a previous hospitalization for detoxification one year earlier, followed by early relapse. He was brought to the emergency department of the Local Health Unit of Coimbra due to an episode of hetero-aggressiveness. At admission, he presented structured delusional ideation, with self-referential and persecutory content, evolving over approximately one year, believing that his ex-girlfriend had joined a gang to rob and harm him. He also reported third-person auditory verbal hallucinations (AVH) and bizarre delusional beliefs (e.g., unusual behavior of his cats due to “magnetization” of the house allowing sound transmission; conviction of constant surveillance through his mobile phone and hidden cameras placed in his home).

During hospitalization, long-acting injectable risperidone 100 mg, oral risperidone 3 mg/day, and olanzapine 20 mg were initiated, with improvement in contact, thought organization, and attenuation of AVH, although residual delusional ideation persisted, along with lack of insight. Additional diagnostic tests were performed to assist in differential diagnosis, particularly regarding non-psychiatric conditions that could manifest with this presentation. Brain MRI revealed an area of frontobasal and left anterior temporal encephalomalacia, with ex vacuo dilatation of the anterior horn of the left lateral ventricle, related to the previous surgical history.

Summary of results: This case illustrates the complexity of differential diagnosis between substance-induced psychosis and primary psychotic disorder, particularly in the presence of persistent psychotic symptoms after abstinence and clinical stabilization. The late age of onset reinforces the need to exclude secondary etiologies, including neurological causes. The history of anterior communicating artery aneurysm suggests a possible substrate of neurobiological vulnerability, potentially associated with frontotemporal dysfunction.

Conclusions

This case illustrates a multifactorial model of transition to psychosis, in which the interaction between genetic predisposition, acquired brain injury, and chronic substance exposure appears to have played a synergistic role in psychotic decompensation. Early identification of high-risk individuals may allow for targeted interventions, with the potential to prevent or delay the development of a psychotic disorder.

References

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