Abstract
Background
Multiple sclerosis has been suggested as a potential vulnerability factor for schizophrenia and other psychotic disorders, and there is a hypothesis about a common etiology in a subgroup of schizophrenia and multiple sclerosis [1]. Immune-related single-nucleotide polymorphisms have been associated with schizophrenia and genetic pleiotropy between schizophrenia and multiple sclerosis has been reported, but not between bipolar disorder and multiple sclerosis (at the level of major histocompatibility complex) [2]. As new data about the involvement of genetically-determined immune factors in the susceptibility to schizophrenia appear (e.g., variants of complement factor 4 possibly linked to synaptic pruning during brain development) [3] the interest for finding therapeutic targets within the immune system for psychotic disorders is also increasing.
Methods
Three patients diagnosed with both schizophrenia spectrum disorders (schizophrenia n=2, or schizoaffective disorder, depressive type n=1), female, mean age 43.7, with a history of psychotic disorder for at least one year, were monitored during 6 months using Positive and Negative Syndrome Scale (PANSS), Global Assessment of Functioning (GAF), Clinical Global Impressions – Severity (CGI-S), Columbia-Suicide Scale for Schizophrenia (CSSRS), Calgary Depression Scale (CDS), Multiple Sclerosis Severity Scale (MSSS), and the Extrapyramidal Symptom Rating Scale (ESRS). None of these patients presented other organic or psychiatric co-morbidity, and they were on active treatment for their multiple sclerosis throughout the 6-month duration of psychiatric evaluation. All patients were initiated on a new antipsychotic, because of the lack of efficacy of the previous agents, or due to their lack of therapeutic adherence. A patient was initiated on olanzapine 15 mg/day, while the other two received risperidone 4 mg/day. The antipsychotic doses were flexible during the 6 months of the treatment, with olanzapine between 10 and 20 mg daily, and risperidone between 3–6 mg daily. The initial PANSS mean score was 92.2, with a GAF of 35.3 and a CGI-S of 5.1.
Results
All patients reached the week 24 visit of their evaluation, and the overall tolerablity of the antipsychotic treatment was good. All patients had lower PANSS scores at week 24 (the mean decrease was -25.6 points compared to baseline), higher GAF scores (+27.7 points), and lower CGI-S (-2.5 points). CSSRS did not change significantly during the 6 months, the score remained at minimum value, and the CDS scores also remained constantly under 3. ESRS recorded transient increments, but at week 12 they were not significantly increased reported at the baseline values, and no corrective medication was recommended throughout the 6 months for extrapyramidal symptoms. MSSS mean score did not change significantly at week 12 compared to its baseline values.
Discussion
Atypical antipsychotics are efficient and well tolerated in patients with schizophrenia and multiple sclerosis dual diagnosis. The positive effects of atypical antipsychotics maintained during the 6 months of monitoring and they had no significant impact over the multiple sclerosis symptoms.
References
Functional outcomes and patient satisfaction following inpatient treatment for childhood‐onset schizophrenia spectrum disorders vs non‐psychotic disorders in children in the United Kingdom