Schizophrenia Clinical Trial
Official title:
A Randomised Trial Examining the Effectiveness of Sympathetic Nervous Inhibition in Alleviating the Metabolic Side Effects of Antipsychotic Medications in Patients With Schizophrenia
The use of antipsychotic medications has increased over the past decade. While more recently
developed medications are improved with regards to extrapyramidal side effects, the use of
atypical antipsychotics has been associated with substantial weight gain and a worsening of
metabolic profile. The time course and extent of weight gain differs among antipsychotics,
with olanzapine and clozapine being associated with greatest weight gain.
Mechanisms underlying a worsening metabolic profile, obesity and obesity-related illnesses
are complex, extending beyond sedentary lifestyle, poor diet and genetic predisposition.
There is also a growing body of evidence that the sympathetic nervous system (SNS) has a role
in the generation of both obesity and obesity-related illness. While the role of the SNS in
blood pressure control is readily acknowledged it is less well appreciated that activation of
the SNS exerts profound metabolic effects.
Although the fact of a causal relation linking antipsychotic drugs and obesity is
unequivocally established, the biological mechanisms operating are unclear, and strategies
for preventive therapy remain largely unformulated.
This study aims to investigate the role of the SNS and its association with the metabolic
abnormalities that are frequently observed in patients with schizophrenia following treatment
with antipsychotic medications.
Additionally, the study will investigate whether treatment with the centrally acting
sympatholytic agent moxonidine will modify SNS activity and, hence, favourably influence the
downstream metabolic abnormalities seen in antipsychotic treated patients with schizophrenia.
Hypothesis 1: Elevated sympathetic nervous system activity underlies the metabolic
disturbances observed in patients following antipsychotic therapy.
Aim 1: To investigate the role of the sympathetic nervous system and its association with the
metabolic abnormalities that are frequently observed in patients with schizophrenia following
treatment with antipsychotic medications
Hypothesis 2: Central sympathoinhibition with moxonidine will blunt the elevated sympathetic
nervous activity and downstream metabolic abnormalities observed in antipsychotic treated
patients with schizophrenia.
Aim 2: Determine whether treatment with the centrally acting sympatholytic agent moxonidine
will modify sympathetic nervous system activity and, hence, favourably influence the
downstream metabolic abnormalities seen in antipsychotic treated patients with schizophrenia.
n/a
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