Structural Brain Modifications in Primary Insomnia: Myth or Reality?

Abstract

965 Editorial—Dang-Vu In comparison to other disorders of sleep, the number of brain imaging studies in chronic primary insomnia remains limited.1,2 The earliest reports in this area utilized functional modalities. In a study using single photon emission computed tomography (SPECT) with 99mTc-hexamethylenepropyleneamine oxime (99mTc -HMPAO), patients displayed decreased perfusion in basal ganglia and various cortical areas during NREM sleep when compared to the same sleep stage in healthy controls.3 Nofzinger et al. then used positron emission tomography (PET) with 18F-fluorodeoxyglucose (18F-FDG) to investigate brain glucose metabolism in primary insomnia patients, during both NREM sleep and wakefulness.4 The main finding of their study was the demonstration that relative to control subjects, patients with primary insomnia showed less reduction of glucose metabolism during the transition from wakefulness to NREM sleep in the brainstem, hypothalamus, thalamus, limbic areas, and medial prefrontal cortex. This result is commonly referred to as supporting the hyperarousal hypothesis in insomnia.5 Using functional magnetic resonance imaging (fMRI), Altena et al.6 assessed brain responses during a verbal fluency task and found that chronic primary insomniacs showed less activation in medial and inferior prefrontal cortices than controls. More recent neuroimaging studies of primary insomnia were exclusively dedicated to structural brain changes associated with this condition. In a pilot MRI study, Riemann et al. investigated volumetric differences in several brain regions of interest between chronic primary insomnia patients and control subjects.7 Only the hippocampus was reduced in volume in their small sample of 8 patients—a finding that did not survive correction for multiple comparisons. In order to reevaluate this hippocampal alteration in insomnia, two other MRI studies used a manual tracing of hippocampal volumes in 20 chronic primary insomnia patients, and both reported no significant decrease compared to controls.8,9 Data from one of these two studies were reanalyzed to focus on another region of interest: the anterior cingulate cortex. Winkelmann et al.10 observed a volume increase of this area in patients, which was confirmed by the same authors on a second independent sample of 21 primary insomniacs, and interpreted as a compensatory response to chronic sleep disruption. Another study performed MRI scans in 24 chronic primary insomniacs and analyzed differEDITORIAL