Background: Bipolar II disorder is a debilitating psychiatric illness with a higher prevalence in the psychiatric population than previously believed. However, little is known concerning the biological underpinnings of the disorder. In recent years, the glutamatergic hypothesis of depression implicating synaptic plasticity and neuronal circuits in the pathophysiology of affective disorders have gained a lot of attention. The current study is a reexamination, with an aim of replicating the results of an initial study which found increased synaptic plasticity in the visual cortex of healthy controls subjects after exposure to prolonged visual stimulation. If this result is replicated, this would contribute in the validation of VEP-methodology as a means of probing synaptic plasticity in human tissue non-invasively. Further aims for the current study is to find differences in synaptic modulation between the patient and control group, and to explore whether severity of depression as measured by MADRS has an impact on the synaptic plasticity of patients. In addition, neuropsychological tests of verbal and visual memory was administered to map cognitive function in the two groups, and explore whether possible neuropsychological impairment had an impact on the measure of synaptic plasticity.
Methods: VEP-recordings were used to probe synaptic plasticity in a total of 33 BP-II patients and 34 healthy control subjects. The participants were screened for previous head injury, a history of neurological or other severe chronic somatic disorders, and pregnancy.
Results: The results demonstrated an increased modulation of synaptic plasticity in the healthy control group. Further results demonstrated a significant difference in synaptic plasticity between the BP-II and control group, and a significant correlation between severity of depressive symptoms and visual synaptic plasticity.
Conclusion: The results from the current study strengthens the validity of the VEP-methodology as an inexpensive and non-invasive method of recording synaptic plasticity in human subjects.
Errata: The scatterplots in Figure 6/Figure 7 page 46/47 were unfortunately included in the thesis by a mistake. The scatterplots are presented with a line showing a perfect correlation between severity of depression as measured by MADRS and synaptic plasticity/test-retest correlations of modulation effect on C1, P1, N1 and P1-N1 peak-to-peak in healthy control subjects, which is misleading. See page 32, 7.6 ”Validity of the VEP-paradigm; comparing initial and current examination” and 7.8. ”VEP plasticity, mood state and psychiatric comorbidity” for a discussion of the results.