Analysis of Sleep Deprivation Effects on Brain and Cognitive Function

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Added on  2019/11/20

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This report examines the impact of sleep deprivation on cognitive performance and brain activity, focusing on the prefrontal cortex and thalamus. The study involved 17 subjects, analyzing brain activity during 85 hours of sleep deprivation. Results showed a decrease in glucose metabolic rate and activity in the posterior parietal cortex and thalamus, correlating with reduced cognitive function. The report also discusses the state instability hypothesis, noting the limitations of the study in fully supporting it due to a lack of analysis of performance variability and compensatory efforts. It highlights the connection between decreased prefrontal cortex activity and vulnerability to extended wakefulness. The report underscores the need for further research involving behavioral data, brain imaging, and analysis of lapses to strengthen the understanding of sleep deprivation's effects on cognitive processes and the state instability hypothesis.
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To what extent is the prefrontal cortex impairment hypothesis supported?
The hypothesis states that sleep deprivation creates negative effects on cognitive
performance and alertness and this is related to brain activity and function decrease. This
decrease in activity occurs in thalamus and the prefrontal cortex which is involved in
attention and alertness and higher-order cognitive processes. The study tested 17 subjects for
changes in brain activity during 85 hours of sleep deprivation. During the 18FDG uptake,
each of which occurred for 30 minutes, the subjects participated in SD serial addition and
subtraction tasks. Polysomnographic analysis revealed that the subjects were awake. The
cerebral metabolic rate for glucose showed a global decrease of 8% and 3-7% more decrease
in regional values after the twenty four hour sleep deprivation stage. The decrease was
observed in posterior parital cortex and the thalamus. A decrease was also observed in the
cerebellar vermis, medial temporal cortex and right ventral cerebellar hemisphere. Moreover,
cognitive performance and alertness showed a decline with the deactivation of brain regions.
Thus, the study provided evidence for substantiating the relation between normal functioning
of the brain and sleep. It also proved that sleep deprivation for a short period decreases brain
activity. The corticothalamic network activity, which controls cognitive skills and attention,
gets reduced significantly. Hence, it proved association between sleep deprivation, reduced
brain activity and decline in cognition.
To what extent is the state instability hypothesis supported by the study?
The state instability hypothesis is supported to a lesser extent. The hypothesis states
that sleep deprivation affects the performances which rely on certain fundamental
neurobehavioral processes that are sensitive to this instability. The hypothesis also states that
attention components like sustaining attention over long periods of time acts as a potential
candidate for the important neurobehavioral processes in the brain and are extremely
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vulnerable to state instability. The study did not attempt to find any correlation between
increase in performance variability and progression of sleep loss. Furthermore, it failed to
provide evidence if an escalation in variability of response occurs due to an increase in
compensatory effort as the sleep loss progresses. The study revealed connections between
deactivation of certain regions of the brain with human sleep deprivation. Its main focus was
to form an association between changes in the CMRglu in prefrontal cortex regions of the
brain with sleep deprivation. It also indicated that decreases in the activity of prefrontal
cortex and posterior parietal cortex are related to a larger biological vulnerability to extended
wakefulness. To perform well on explaining the hypothesis, many other parameters like
analysis of the lapses that occur, behavioral data studies and brain imaging studies that show
correspondence with fast and slow responses after a normal night of sleep should have been
involved. Thus, the parameters of cortical association studies are not sufficient to demonstrate
any connection between state instability hypothesis and increase in sleep drive.
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