2 research outputs found
Basal ganglia structure and the effects of neuroleptic treatment in schizophrenia
Schizophrenia is a complex mental illness of unknown etiology. Clinical
research has suggested that abnormalities of the basal ganglia are present in
schizophrenia. Whether these abnormalities are present at the beginning of
illness or progress with time remains controversial. Concomitantly,
antipsychotic treatments, particularly traditional neuroleptics, may exert
metabolic effects on the basal ganglia, but the effects of new atypical
antipsychotic are unknown. To elucidate the nature of underlying basal ganglia
structure and the effects of antipsychotic treatment on striatal morphology,
clinical signs and symptoms, three MRI studies of basal ganglia volumes were
conducted.
In study A, baseline volumes in a cohort of drug-naive first episode
psychosis (FEP) patients, chronically treated schizophrenia patients and
healthy controls were assessed. Chronically treated patients had larger basal
ganglia volumes compared to both never-medicated patients and healthy
controls. Never-medicated patients' basal ganglia volumes were not different
from controls.
In study B, extrapyramidal symptoms (EPS) and their relationship to
neuroleptics and striatal volumes were examined. Prior to neuroleptic
treatment, 39% of FEP patients had EPS at baseline. FEP patients who
presented with parkinsonism had larger left caudate volumes than those who
did not. In study C, the effects on basal ganglia volumes and EPS after switching
patients from risperidone or typical antipsychotics to olanzapine were
examined. Patients previously treated with typicals had decreases in putamen
and globus pallidus volume after switching. Patients previously on risperidone
had a decrease in caudate volume after switching. Patients maintained on
risperidone had no changes in basal ganglia volumes. Severity and prevalence
of EPS were unchanged after switching.
No underlying volumetric abnormalities of the basal ganglia in drug-naive
first-episode schizophrenia were observed in the cohort of patients
included in this thesis. However, movement disorders were seen in a notable
portion of drug-naive schizophrenia patients, suggesting that abnormalities of
the basal ganglia or circuits of the basal ganglia are present and may be subtle.
Atypical neuroleptics do not induce additional EPS at clinically effective
doses. Chonic exposure to atypical neuroleptics is not associated with striatal
hypertrophy, and in the case of olanzapine, may reduce caudate volumes in
some patients.Medicine, Faculty ofGraduat