Schizophrenia is a major health problem in which diversification and increase in the quality of antipsychotic molecules did not yield the anticipated results. that the etiopathogenesis of schizophrenia accounts for a combination of genetic factors forming the genetic spectrum of vulnerability for schizophrenia. The neurodevelopmental anomalies correlated with the gestational period and obstetric traumatisms raises major pharmacological management issues. The two levels of vulnerability (genetic and neurodevelopmental) are the basis of the pathogeny of side effects induced by antipsychotic medication. The most severe side effects are related to extrapyramidal symptoms, hyperhomocysteinemia, hypofrontality, impairment of the neurovascular unit and neuronal metabolic processes. Understanding these particular mechanisms will allow the clinician to identify the pathogenic model of schizophrenia, customized for each specific case. The adverse drug reaction decreases the compliance and adherence to the treatment, determining repeated discontinuations with psychotic relapses, and may trigger psychopathogenic bursts deteriorating the structural and cerebral functional balance. The type of psychotropic medication must be taken into account, as well as the concomitant medication administered for comorbidities associated with schizophrenia. The cerebral vascular modifications are correlated with the metabolic syndrome induced by antipsychotic medication. This complex syndrome, associated also with modifications in the homocysteine metabolism, determines weight gain, obesity, high blood pressure, ischemic cardiopathy, hyperglycemia and dyslipidemia. Identification of possible biological or neuroimaging markers helps and their early correction may prevent the onset of neurodegenerative evolution and irreversible cerebral atrophies, as well as decrease the risk of side effect that may endanger the life of the schizophrenic patient. The complexity of the pathogenic mechanisms requires a prophylactic behavior, not based on therapeutic switch, but on the proactive, customized pharmacologic intervention, addressing the pathogenic chains.

Adverse reactions to psychotropic medication can be considered as risk indicators for an unfavorable evolution of patients with schizophrenia, based on particular pathogenic mechanisms that can be used in the personalized therapeutic approach. The combination of antidepressants with antipsychotic drugs in schizophrenia has a risk of synergistic action of excessive blockade of dopamine receptors, which causes hyperprolactinemia. Primary hyponatremia occurs during pregnancy and can be an important marker for signaling neurodevelopmental abnormalities, while secondary hyponatremia has a major clinical dimension and is induced by psychotropic drugs. The pathogenic mechanisms presented can be objectified by neuroimaging examinations that bring benefits in the diagnostic accuracy and re-evaluation of the therapeutic approach, especially in correlation with the severity of biological markers such as prolactin and sodium. The persistence of high prolactin and low sodium levels is an alarm signal that announces a negative evolution of the patient or a major risk of severe cardiac, metabolic, vascular or renal comorbidities. Recognition of pathogenic mechanisms of neurodevelopment, including ventriculomegaly, hyponatremia, focal cortical dysplasia, hippocampal or temporal lobe lesions, in association with a positive history of neonatal or febrile seizures, requires prophylaxis due to high risk of onset of schizophrenia in childhood. Fetal cortical dysplasia is associated with the risk of neonatal seizures. This vulnerability favors the appearance of febrile convulsions or enuresis with changes in brain structure. Enuresis may be an important marker of neurodevelopmental potential for schizophrenia. Neonatal seizures are correlated with hyponatremia and severe hypertension, which appeared in the third trimester of pregnancy, can trigger eclampsia. Neuroimaging monitoring in patients with neurodevelopmental abnormalities, hyperprolactinemia and primary or secondary hyponatremia, acquires a major importance, being able to delimit the boundary between a functional lesion, potentially reversible, with an irreversible lesion.