Amber Badgerow
November 5, 2011
PSY 213
John Olmsted
A Neurobiological Look at Insomnia
Question:
Insomnia is a troubling sleep disorder that permeates almost all aspects daily life. Its effects go beyond fatigue. What are some of the underlying mechanisms of insomnia? How is the brain involved?
Prediction:
Hormones and neurotransmitters may play a part in insomnia- causing a person to become unable to fall asleep or remain asleep. The brain is possibly more active while sleeping in those with insomnia and therefore is less able to shut out stimuli.
Article 1: “Reduced Brain GABA in Primary Insomnia: Preliminary Data from 4T Proton Magnetic Resonance Spectroscopy (1H-MRS)”
This article was written by John W. Winkelman, MD, PhD, Orfeu M. Buxton, PhD, J. Eric Jensen, PhD, Kathleen L. Benson, PhD, Shawn P. O'Connor, BA, Wei Wang, MA, and Perry F. Renshaw, MD, PhD to discuss their study conducted to examine GABA levels, using proton magnetic resonance spectroscopy (1H-MRS), in subjects with primary insomnia. Insomnia is the most common sleep disorder- about 10% of all adults in industrialized countries are afflicted. Primary insomnia is that without accompanying medical conditions and affects approximately 25% of those with insomnia. They reasoned that GABA levels could be involved in insomnia because it is an inhibitory neurotransmitter that reduces electrical activity to help brain regions shut down for sleep. Winkelman et al. recorded GABA levels in the central region of the brain, which included the thalamus, the basal ganglia, and the temporal, parietal, occipital, and frontal white-matter and cortex. The study found that subjects with primary insomnia had an almost 30% reduction in average GABA levels compared to the control group of well-screened normal sleepers. Furthermore, both the inability to maintain sleep and overall sleep quality correlated with GABA levels. Since subjects were tested during the day, the results supported evidence from other studies that primary insomnia is associated with hyperarousal. This study indicated that reduction of GABA is one of the neurobiological mechanisms of insomnia.
Article 2: “Regional Cerebral Metabolic Correlates of WASO During NREM Sleep in Insomnia”
Eric A. Nofzinger, M.D., Christoph Nissen, M.D., Anne Germain, Ph.D., Douglas Moul, M.D., Martica Hall, Ph.D., Julie C. Price, Ph.D., Jean M. Miewald, B.A., and Daniel J. Buysse, M.D. studied the relationship between wakefulness after sleep onset (WASO) in subjects with primary insomnia and regional cerebral metabolism during non-rapid eye movement (NREM) sleep. Nofzinger et al. evaluated regional cerebral glucose metabolism using [18F]-fluorodeoxyglucose (FDG) positron emission tomography (PET) to measure metabolic activity. Results showed that cortical metabolism increased in the frontal cortex, pontine tegmentum, thalamus, temporal cortex, and anterior cingulate cortex in association with increased WASO (both subjective and objective) during NREM sleep. Findings from other studies on brain activity and insomnia that used different methods also demonstrated hyperarousal in insomnia. The increased WASO in correlation to increased glucose metabolic activity in the brain could indicate that subjects with insomnia had increased activity in higher level cognitive processes- associated with emotional awareness, fear, conflict monitoring, goal-directed behavior, and anxiety- and/or in arousal systems during NREM sleep.
Source Validity:
Both sources had credible authors and matched subjects well for age and race. The subjects in the first study had not been medicated and did not have a history of mood/anxiety disorder. The subjects in the second study were tested for drugs and preexisting mood disorders. Both sources screened subjects for insomnia and the specifics of insomnia- sleep diaries were obtained and polysomnographic assessments done to get an objective view of the subjects’ sleep. However, small sample sizes greatly reduce the reliability of the results in both studies (sixteen in the first and fifteen in the second). The first article also mentioned that the method used not produce anatomically specific findings and that the lack of EEG or behavioral monitoring of subjects could have resulted in interference from the behavioral state of the subjects. Although the second article had many other studies to reference from, the first study has yet to be repeated to ensure accurate results.
Reflection on Hypothesis:
The research discussed supports my hypothesis that insomnia is related to levels of certain neurotransmitters and increased brain activity. More research must be gathered to confirm that hormones are involved in insomnia and that increased brain activity in those with insomnia causes decreased ability to block external stimuli.
Works Cited:
Winkelman John W., Buxton Orfeu M., et al. “Reduced Brain GABA in Primary
Insomnia: Preliminary Data from 4T Proton Magnetic Resonance Spectroscopy
(1H-MRS).” Sleep 31.11 (2008): 1499–1506. Associated Professional Sleep
Societies, LLC. EBSCOhost. Web. November 5, 2011.
Nofzinger Eric A., Nissen Christoph, et al. “Regional Cerebral Metabolic Correlates of
WASO During NREM Sleep in Insomnia.” Journal of Clinical Sleep Medicine 2.3
(2006): 316-322. The American Academy of Sleep Medicine. GoogleScholar
(“metabolic brain activity insomnia”). Web. November 5, 2011.
My mother gave me these supplements. They have GABA in them. I have always had insomnia. Mostly from school stress. I like that I could read the second article and infer that it meant that I had higher cognitive processing. Ha!
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