Brain Stimulation and Treating Mental Illness

 

When medicine speaks the body’s language

When medicine speaks the body’s language

Most of modern medicine focuses on creating synthetic drugs in a lab, from more synthetic ingredients; treating some issues while creating new ones. Scientists Wei-Ming Yu, Madelyn A. McCullen, and Vincent C.-F. Chen explored a different approach when looking at nerve injuries by using electricity itself as the course of treatment. They mainly focused on peripheral nerves because of their role as information transmitters through electrical signals between central and peripheral nervous system, functioning as the brain’s own language. 

However, this is not the first time electricity has been used a form of treatment. Historically, other forms of electrical stimulation have been used, such as electroconvulsive therapy (ECT), which alters brain activity to simulate seizures. What makes this new study special is the fact that instead of focusing on intensity and frequency, it emphasized how the pattern of electrical stimulation influences the body’s response.  

In the case of peripheral nerves being damaged, communication between the brain and the rest of the body is affected which often leads to a loss of sensation or motor function. Because these nerves are highly dependent on electrical signals, the researchers have explored electrical stimulation as a way to restore communication and promote the regeneration of these synapses. Instead of increasing the strength or frequency of signals are delivered, the scientists suggested that the structure of the signal itself is what actually mattered.  

Ultimately, this study highlighted a shift in how medicine approaches treatment and healing by using the body’s own language. Why introduce new chemicals into the human body when the body already has successful ways of healing itself, all science needs to do is enhance these systems. 

References

Yu, W.-M., McCullen, M. A., & Chen, V. C.-F. (2022). Accelerating peripheral nerve regeneration using electrical stimulation of selected power spectral densities. Neural Regeneration Research, 17(4), 781–782. https://doi.org/10.4103/1673-5374.322458

Zhang, M. W. B., & Ho, R. C. M. (2019). Electroconvulsive therapy: Current perspectives. World Journal of Psychiatry, 9(1), 1–12. https://doi.org/10.5498/wjp.v9.i1.1

Drugs Rewire the Brain

In our generation, drugs are a concerning problem, becoming more and more common among today's youth. Modern society faces a growing challenge with substance abuse disorders, including stimulant and opioid addiction. Drugs do not simply create social pressure, but rewire and change neural pathways responsible for desire, motivation, and self-control. Cocaine addiction in particular remains a serious concern as it is responsible for altering the reward system in ways that increase cravings and decrease our ability for self-control. 

Dr. Stephan Steidl and colleagues explored this in their lab, specifically looking at pathways in the laterodorsal tegmental nucleus and ventral tegmental area. They examined how repeated cocaine exposure changes communication in the reward circuitry of the brain. Through their experiments, they studied glutamate signaling in the VTA, displaying that cocaine strengthens excitatory inputs to dopamine neurons through mechanisms like LTP. They used ontogenetic techniques and found the role of LDTg glutamate cells or their VTA afferents to be essential in the development of cocaine sensitization in male mice. They discovered that the connection between the laterodorsal tegmental nucleus and the ventral tegmental area is required for the sensitization of cocaine. Sensitization occurs when repeated drug use causes the brain to react more strongly to cocaine over time, which increases behavioral responses and reinforces addiction pathways. Repeated drug use over time leads to sensitization, the brain becomes more responsive to the drug use, and results in enhanced drug-seeking behaviors and relapse.

These studies were done on male mice; another closely related study, "Cocaine self-administration disrupts mesolimbic dopamine circuit function and attenuates dopaminergic responsiveness to cocaine," looked at what happens to the brain when humans use cocaine. Researchers in the lab of Dr. Jones in the Department of Physiology and Pharmacology at the Wake Forest School of Medicine used machines like PET scans to see how cocaine affects the dopamine pathways in people who are addicted to it. They found that people with chronic cocaine use showed reduced dopamine receptor availability and abnormal reward processing in the mesolimbic system. These structural changes make natural rewards, such as relationships, achievements, and hobbies, less satisfying, while drug-related cues become more powerful triggers for cravings. Things that are normally fun, like spending time with friends or doing something you're good at, are not as enjoyable anymore.

Together, these studies shift the concern from a societal issue to a biological issue. This reinforces the behavior addicts display and how it is difficult to reverse the effects caused by cocaine and other such drugs. Such studies inform us, the public, of the biological effects of addiction and how they actively rewire it. Drugs are a measurable condition that reshape neural pathways over time, and if not taken precautions against, will ruin every generation that abuses them. 

Works Cited: 

Siciliano CA, Ferris MJ, Jones SR. Cocaine self-administration disrupts mesolimbic dopamine circuit function and attenuates dopaminergic responsiveness to cocaine. Eur J Neurosci. 2015 Aug;42(4):2091-6. doi: 10.1111/ejn.12970. Epub 2015 Jun 28. PMID: 26037018; PMCID: PMC4540675.

Steidl, S., Wang, H., & Wise, R. A. (2017). Glutamate inputs from the laterodorsal tegmental nucleus to the ventral tegmental area are essential for the induction of cocaine sensitization in male mice. Neuropsychopharmacology, 42(11), 2232–2241. https://doi.org/10.1038/npp.2017.72

Is it ADHD Or Just Sleep Debt?

    The review article "An update on adolescent sleep: New evidence informing the perfect storm model" by Stephanie Crowley et al. discusses current understanding about adolescent sleep patterns and the consequences of them. There is a section that highlights the circadian barrier that comes from early start times in high school, especially being shifted after middle school. A key finding was "that the melatonin onset phase (i.e., the circadian timing system) for these adolescents was 40 min later in 10th versus 9th grade" (Crowley, 2018). 10th graders experience a natural shift in their circadian system that makes them feel tired 40 minutes later than their younger selves, and therefore require a later wake time to make sure they get enough sleep. So, to suit their biology, 10th graders should have later school start times than previous years, but instead they have even earlier ones! When their biology says that they should be sleeping at a certain time in the morning, it can not be constructive to have a student instead sitting in a classroom trying to learn content; their brain should still be resting. Having this disconnect in so many young people naturally leads to behavioral and cognitive consequences, so as time has progressed to have so many students in this position, it makes sense that more behavioral and cognitive performance issues are popping up too. As these school times as well as many other psychosocial pressures weigh on adolescents and drive them into sleep dept, there could be major decreases in focus, attention, and academic performance as a result.

    Lacking in focus, attention, and academic performance are all common traits of ADHD and other behavioral disorders. In the past decade, there has been a major increase in the diagnoses of these conditions, and many more outwardly wondering if they may have one of these disorders. 

    On the topic of ADHD, I read the Neuroscience article "Prior Sleep and Age Sculpt the Brain’s Awake Signals" that discusses a research paper that analyzed young people and sleep in a different way than the article I've already discussed. It was discussed here that expected differences are to be seen in the brain activity of ADHD and neurotypical children, and the previous research in the field found activity differences between the sleeping brains of ADHD children compared to neurotypical children. However, when this research was conducted on their waking brains, the same differences were not observed. This suggests that the observed differences are not due to the disorder itself, but must be something else related to the sleep quality of these children. The question then becomes, what caused the differences in brain activity between different children while they were sleeping that didn't occur while they were awake? Additionally, these findings when they were sleeping were such a way that they were accepted as explained by the disorder, and only further research discovered differently. More work is needed to be done to be sure, but the article suggests that these differences could be caused by sleep dept and the outcomes that it leaves on an individual, sleeping and awake. When it comes to children with ADHD and those without, "the variability in their brain signals... suggests that many observed brain patterns may actually be signals of sleep debt rather than the disorder itself," (NeuroscieneNews, 2026).

    The connection I made when reading both of these articles may be a bit of a stretch, but it is a potential connection that could be a target of future research. With the research about adolescent sleep quality and subsequent consequences in their academic and personal lives, I wonder if these results are being observed more frequently than expected over these past couple decades. Something I know has been increasing in diagnoses and frequency in society is ADHD and other behavioral disorders. I have heard a lot of skepticism over conditions like this because of how much they are popping up, and how they seem to affect too many people. Based on both of these papers, I think it is possible that this increase in behavioral disorder prevalence is related to the decrease in sleep quality across so many adolescents these days. If there are a lot of young people who are experiencing behavioral difficulties, especially in school, yet it seems to be totally normal and something they can't change, it may be due to the normalization of such pressure filled lives and our society that expects sleep to be sidelined for other priorities. If the sleep dept is normalized to an individual, then their behavior is also normalized, at least in the sense that it is seen as an innate part of the individual rather than just a consequence of struggling at a particular time. Whether or not this sleep-disorder correlation is true, I think it simply highlights the importance of getting a comprehensive and professional opinion of ones behavior, if possible, if there are ever concerns of typical and atypical behavior. Maybe an individual is struggling in many similar ways as someone with ADHD, but they can improve based on just their environment, which is a solution that people who really do have the disorder no not have. This further research could assist in understanding adolescents more and realizing the depth of pressure they are under, and this can lead to better assistance and intervention for those who are struggling, behavioral disorder or not.

References: 

Crowley, Stephanie et al. "An Update on Adolescent Sleep: New Evidence Informing the Perfect Storm Model." Elsevier, 2018.

Neuroscience News. “Prior Sleep and Age Sculpt the Brain’s Awake Signals.” Neuroscience News, 27 Apr. 2026, neurosciencenews.com/awake-eeg-sleep-brain-development-30614/

The Effects of Physical Exercise on Sleep Before Sleep

 The Effects of Physical Exercise on Sleep Before Sleep

    Recent studies have shown that being able to have a good nights sleep is immensely beneficial for physical performance. Hitting more that 8-9 hours for an adult is considered the perfect amount of sleep. With physical performance, sleep is critical for physical performance. It’s when the body repairs muscle tissue, restores energy stores, and regulates hormones that control strength, endurance, and recovery. Poor sleep can lead to slower reaction times, reduced coordination, and quicker fatigue, making workouts feel harder and increasing the risk of injury. On the other hand, consistent, high-quality sleep supports better focus, faster recovery, and improved overall athletic output, meaning you not only perform better but also adapt more effectively to training over time. Many people have tried even exercising right before bed thinking that exercise at not matter the time of day would make them tired enough to go to sleep and get a good amount of sleep. According to Alnawwar et. al, extreme exercise before bed actually has detrimental affect on your sleep. Like all other healthy actions, everything is good in moderation. Extreme sleep before bed can disrupt sleep. High intensity workouts within 1-4 hours of sleep can raise core body temperatures, increase heart rate, and release adrenaline which can make it much harder to sleep. Light exercise like a jog can make you much more relaxed, however, lifting heavy weights, sprinting, or many other things can cause you to not be able to sleep. It is recommended by most doctors to keep late night exercising to a maximum of 30 minutes. It is an interesting discovery but can bring insight to those who feel like they struggle to fall asleep even though they seem to be tiring themselves out before bed. 

Works Cited

Alnawwar, Majd A., et al. “The Effect of Physical Activity on Sleep Quality and Sleep Disorder: A Systematic Review.” Cureus, vol. 15, no. 8, 16 Aug. 2023, pmc.ncbi.nlm.nih.gov/articles/PMC10503965/, https://doi.org/10.7759/cureus.43595.

‌

It Isn't Just Willpower: The Brain Science Behind Overeating

    Overeating is often reduced to a failure of impulse control, where individuals ignore their body's satisfaction cues by eating past the point of feeling full. However, this oversimplification overlooks the underlying neurological process where physiological signals in the brain’s reward center are activated before eating begins, which contributes to loss of control eating. In Joe Vukov’s research paper titled “ Brain-Responsive Neurostimulation for Loss of Control Eating: Early Feasibility Study,” loss-of-control (LOC) eating is referred to as the feeling of being unable to stop eating or regulate how much one consumes.   

    After analyzing this study, the most interesting point was made about LOC eating and how it isn't about willpower but is interlinked with the brain’s reward system, specifically the nucleus accumbens, which responds to anticipating food rather than just the action of eating. Vukov suggests that there are small windows occurring before a person eats, where the brain is already signaling that a loss of control occurrence is about to take place. The proposed solution is to use the brain's responsive neurostimulation to interrupt the signal before the urge becomes an eating behavior. 

    These findings correlate with a Psychology Today article titled Loss of Control Eating After Metabolic and Bariatric Surgery by Riccardo Dalle Grave, which explains how, after a metabolic or bariatric surgery, people can still experience this loss of control eating because the underlying brain-driven urge and patterns are unchanged. Ultimately, these surgeries only alter the stomach and not the reward system that pushes these compulsive food eating behaviors. His findings provide more insight into why some patients experience a regain of weight post surgery because of the ongoing neural pattern.

    Both sources clarify how complex the issue of overeating really is because a person’s brain is already driven by the behavior before they consciously decide to eat. This means treatment only focuses on behaviors such as diet or stomach reconstruction and may ignore the underlying issue. Therefore, developing approaches that target the brain will be more effective for some people. Overall, it is abundantly clear that the loss of control behavior while eating isn't inherently a bad habit but a neurologically driven process. Once we address the root cause of these stigmatized behaviors, it will feel less productive to blame the individual and more effective to focus on treatments. 

References:

GraveRiccardo. “Loss of Control Eating after Metabolic and Bariatric Surgery.” Psychology Today, 2024, www.psychologytoday.com/us/blog/eating-disorders-the-facts/202409/loss-of-control-eating-after-metabolic-and-bariatric-surgery. Accessed 30 Apr. 2026.

Wu, Hemmings, et al. “Brain-Responsive Neurostimulation for Loss of Control Eating: Early Feasibility Study.” Neurosurgery, vol. 87, no. 6, 27 July 2020, pp. 1277–1288, https://doi.org/10.1093/neuros/nyaa300.

Localizing the Homeostatic System of Sleep

    Sleep and sleep optimization have been areas of interest for years. People seek to learn how to maximize their sleep, what constitutes “good” sleep, and the long-term effects of poor sleep. One such researcher in this field, Dr. Stephanie Crowley, delivered a talk this semester about the effects and potential causes of poor sleep among adolescents. As children grow, their circadian rhythms shift later and later, their “biological night” shifting back much farther into the evening. This shift in sleep schedule, coupled with various sources of pressure, creates what Dr. Crowley dubs a “perfect storm” of chronic sleep deprivation. According to the work of Dr. Crowley, such sources include early school start times that are incongruous with their later biological schedule; social stressors; and an increased sensitivity to evening light that makes it more difficult yet to fall asleep.

    It is believed that sleep quality and sleep schedules are generally regulated by two components: the circadian system and the homeostatic system. The circadian system cycles approximately every 24 hours and is generally consistent regardless of prior sleep/wake conditions. It is more dependent on the time of day and exposure to light. In contrast, its counterpart, the homeostatic system, is quite dependent on prior sleep/wake conditions. It favors sleep the longer one is awake, and favors wakefulness if one has been asleep for a sufficient period. What is most fascinating is the seemingly multimodal nature of the homeostatic system. The circadian system has been localized to the suprachiasmatic nucleus of the hypothalamus; the homeostatic system, however, does not have a single localized center. Instead, it is hypothesized that it synthesizes inputs from many areas of the brain, including but not limited to the nucleus of the solitary tract; the parabrachial nucleus; GABAergic neurons in the medulla; cholinergic neurons in the nucleus ambiguous; and catecholaminergic cells in the ventrolateral medulla and locus coeruleus that work together to regulate sleep-wake states.

    Each of these areas interfaces with the others to promote restful sleep and regulate arousal in the event of danger while one is asleep. For example, the parabrachial nucleus, which serves as the brain’s alarm system and receives inputs from the NST, is primarily known for its arousal-promoting functions. However, a subset of PBN neurons—Adycap1-expressing NST-to-PBN projections—directly promote NREM sleep, thus implicating it as having a much more significant role in sleep-wake regulation. Additionally, the norepinephrinergic locus coeruleus neurons found in the dorsal pons are highest during active wakefulness and absent during REM sleep. The activity of these neurons is crucial for regulating attention and arousal, but sleep-promoting neurons can suppress them via GABAergic inhibition.

    

    The homeostatic system needs many parts to function as smoothly as it does. As someone keen on learning and memory, it would be very interesting to find out the downstream effects of the dysfunction of these areas of the brain, as it has been long established that chronically poor sleep impairs both.

Works Cited

    Yao, Yuanyuan, and Yang Dan. “Body-Brain Integration: The lower brainstem in sleep-wake regulation.” Annual Review of Neuroscience, 20 Apr. 2026, https://doi.org/10.1146/annurev-neuro-082625-012115.

    Crowley, Stephanie J., et al. “An update on adolescent sleep: New evidence informing the perfect storm model.” Journal of Adolescence, vol. 67, no. 1, 13 June 2018, pp. 55–65, https://doi.org/10.1016/j.adolescence.2018.06.001.