http://www.healthimaging.com/topics/diagnostic-imaging/anti-anxiety-medications-change-brain
Benzodiazepines—the
family of popular sedatives that includes Valium and Xanax—seem to
bring about structural changes in the brain, according to a European
study running in the August edition of Psychiatry Neuroimaging.
Sanna Huhtaniska, MD, of the University of Oulu in Finland and colleagues describe their work assessing brain MRI scans from 38 persons with schizophrenia at 34 years old and then again at 43 years old.
Stating their belief that theirs is the first neuroimaging study to home in on “benzos” in the brain, the authors report they found that higher long-term benzodiazepine use associated with reductions in the volume of the caudate. This held even after adjusting for illness symptom scores and cumulative use of antipsychotic medications.
The team also found that, when taking into account illness severity measures and benzodiazepine dose, higher long-term use of antipsychotic meds was associated with increases in lateral ventricular volume.
The authors acknowledge that their work focused on a small sample and did not take into account numerous possible confounding factors such as alcohol use, physical activity levels and nonpharmacological interventions.
They cite as strengths their use of comprehensive, thoroughly collected medication data—they drew from the general-population Northern Finland Birth Cohort 1966 study—and their subjects’ accessing of clinical services in naturalistic rather than research settings.
Huhtaniska and team urge caution in interpreting their findings. The ventricular enlargement they observed in association with antipsychotic medications “may be a marker for a factor we are unable to identify,” they write.
Meanwhile, their finding of caudate reduction associated with cumulative benzodiazepine medication necessitates more studies, they state.
Sanna Huhtaniska, MD, of the University of Oulu in Finland and colleagues describe their work assessing brain MRI scans from 38 persons with schizophrenia at 34 years old and then again at 43 years old.
Stating their belief that theirs is the first neuroimaging study to home in on “benzos” in the brain, the authors report they found that higher long-term benzodiazepine use associated with reductions in the volume of the caudate. This held even after adjusting for illness symptom scores and cumulative use of antipsychotic medications.
The team also found that, when taking into account illness severity measures and benzodiazepine dose, higher long-term use of antipsychotic meds was associated with increases in lateral ventricular volume.
The authors acknowledge that their work focused on a small sample and did not take into account numerous possible confounding factors such as alcohol use, physical activity levels and nonpharmacological interventions.
They cite as strengths their use of comprehensive, thoroughly collected medication data—they drew from the general-population Northern Finland Birth Cohort 1966 study—and their subjects’ accessing of clinical services in naturalistic rather than research settings.
Huhtaniska and team urge caution in interpreting their findings. The ventricular enlargement they observed in association with antipsychotic medications “may be a marker for a factor we are unable to identify,” they write.
Meanwhile, their finding of caudate reduction associated with cumulative benzodiazepine medication necessitates more studies, they state.
“There
is a need for understanding the mechanisms behind antipsychotic- and
benzodiazepine-related structural and functional changes in the brain,”
the authors write. “Further studies should also focus on how
medication-related structural alterations correspond to cognition and
functioning.”
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