The Effects of Music Therapy on Neurological Disorders

I. Introduction

Michael Schneider experienced not one, but two traumatic brain injuries during his lifetime. In 2005, he injured his brain in a helicopter accident. Following that, he experienced decompression when training at a high altitude, which resulted in a stroke. Michael had lost all feeling on the right side of his body. While he did recover, nine years later, he continuously experienced seizures. Additionally, he was diagnosed with PTSD and depression. At this point, Michael had lost all hope; he was certain that he would not make it through the next few years. However, he was then sent to a music therapist who encouraged him to play a few notes on the piano. This was just the beginning of Michael’s journey through musical exploration. He started opening up about his struggles, and said that “It was able to open up all these new pathways through my brain.”⁵

Music therapy is defined as utilizing different components of music as a clinical treatment method. However, it has not always been a popular concept. In the 1940s, Everett Thayer Gaston, now known as the father of music therapy, researched the benefits of music therapy on mental health. In 1968, he concluded that “music therapy follows the path of a behavioral science.”³ Additionally, he claimed that a music therapist’s main goal is to develop an interpersonal relationship with a patient in order to observe the patterns in behavior change.

Music therapy is found to affect three main sections of the brain: the cerebellum, frontal regions, and the hippocampus. The cerebellum is a small section of the brain that controls movement and several motor functions. Because it is connected to the limbic system, which controls emotions, the cerebellum perceives music with a strong production of rhythm and evokes emotional reactions. The neurodegenerative disease, Parkinson’s Disease, is analyzed in this paper to understand the role of rhythm production on the cerebellum in patients who have Parkinson’s.²

The frontal region or the frontal lobe is the largest lobe in the brain and is the most impacted during injury. It controls cognitive functions which are arguably the most important responsibility of the brain. Cognitive functions can range from memory recollection to performing daily tasks. Typically, during traumatic brain injuries, the frontal lobe is the first to be impacted and faces the most damage; this review paper will examine patients with traumatic brain injury and those who experience frequent strokes.

Lastly, the hippocampus is a component of the limbic system, indicating that it controls social functions and the processing of emotions. Because of this, listening to music has been shown to trigger positive emotions and reactions in the limbic system. Mood is a relatively newer topic in its correlation with music therapy due to the constantly changing nature of the limbic system and hippocampus. However, this review paper will discuss a case study performed on patients with Autism and the positive impact of musical components.

Through the several case studies that were performed, researchers have come to the conclusion that music therapy has a multitude of positive effects on the brain and neurodegenerative disorders, especially on movement, cognition, and mood. This review paper will explain the components of music therapy that impact the brain and will
use case studies to support this claim.⁶

II. Cerebellum

A. Anatomy & Physiology of the Cerebellum

The first aspect of neurology that music therapy affects is movement. The cerebellum, frequently known as the “little brain” because of its small size compared to the cerebrum, serves as the central processor for motor functions, hence, affecting movement. To ensure coordination and the accuracy of movements, the cerebellum receives information from the spinal cord and other sensory regions. Next, the sensory information is processed which then translates to controlling motor functions. Additionally, the auditory system is closely connected to the cerebellum, therefore helping to control movement, particularly with automatic responses. However, if the cerebellum were to be damaged, then the loss of functions, including balance and posture, would occur.⁴

B. Effects of Music on the Cerebellum

Neuroscientists have found that music can morph the brain, especially within the motor and auditory regions, by either forming new pathways within the brain, or reinforcing preexisting pathways, all to heal the brain. Listening or even creating music activates motor regions, such as the cerebellum, and results in functional movement. Furthermore, music can be tailored to a particular individual, resulting in the activation of specific neural pathways. Particularly, the cerebellum controls timing of motor functions, specifically processing rhythm. This indicates that music can be altered based on the rhythmic nature to encourage movement in patients. These neural networks are then trained to control fine motor functions, and increase movement within patients who experience a loss of control over motor function.⁸

C. Case Study on Patients with Parkinson’s Disease

To test this hypothesis, a case study was conducted on patients with Parkinson’s disease. Neuroscientists wanted to test if a patient’s control over motor functions would increase if rhythm and timing were altered in music.

Parkinson patients were asked to synchronize their speed of walking to rhythmic cues. As soon as patients coordinated their movement with rhythmic cues, they were able to not only walk faster, but exhibit more control over their bodies. Their neuromuscular activation, limb coordination, angle extensions were more consistent as well. Not only did altering rhythm increase coordination in Parkinson patients, but also maintained consistency in their movement. Furthermore, this improvement was far more drastic than anything that physical therapy could have done. This led to the conclusion that changing components such as rhythm and timing in music can improve motor functions in not only patients with Parkinson’s disease, but also patients who struggle with control over movement.⁹

III. Frontal Region

A. Anatomy & Physiology of the Frontal Region

The second aspect of neurology that is affected by music therapy is cognitive functions. The frontal region, as the name indicates, is located at the front of the brain. It serves to control higher-level functions such as attention, planning, memory formation, and most importantly, speech. A particular cortex, known as the prefrontal cortex, is located in the frontal region. The prefrontal cortex plays a major role in decision-making and any executive functions. To do this, it initiates appropriate behavioral responses in order to interact with the environment surrounding it by evaluating different sources of information. By doing this, the prefrontal cortex is able to control decisions when faced with challenging streams of information. Furthermore, it sends signals to other regions of the brain to assist the prefrontal cortex in making executive decisions. However, the prefrontal cortex also takes longer to develop, which also contributes to more impulsive decisions made at a younger age. Additionally, since it plays a vital role in memory creation, it’s one of the first areas to be affected by degenerative diseases such as dementia and Alzheimer’s.⁴

B. Effects of Music on the Frontal Region

More research has been done on the connections between music and the prefrontal cortex, and scientists have determined that patients who have dementia can recognize songs that hold some significance to them. This is because certain regions of the prefrontal cortex that monitor musical endeavors shut down. However, regions that trigger initiation increase their activity.

C. Case Study on Memory

To further their claim that music therapy strengthens cognitive functions, scientists tried to figure out if specific music exercises would impact cognitive functions such as speech through neuroplasticity. However, this connection was not as obvious as the effect of rhythm on motor functions. Scientists began with two key ideas to explore this concept further: the sharing of functions and the development of the auditory system. The first insight states that the brain’s underlying music is used to share with other functions of the brain. This would mean that music stimulates speech and other cognitive function regions differently than other systems. There are two ways music can stimulate the brain: bilaterally or on the right hemisphere more than the left. For example, in injuries that occur solely on one hemisphere of the brain, music is able to form more flexible neural pathways to either strengthen or relearn functions. In a memory study that was conducted by scientists, word lists embedded in song activate the frontal region as well as the temporal lobe, in contrast to only word activities without music, which activates only the left hemisphere. This shows that music therapy involving elements of spoken-word can enhance several regions of the brain, compared to conventional therapy. Moreover, music can stimulate both neural networks on both hemispheres of the brain which was shown to increase attention span which is often decreased in patients who have experienced traumatic brain injuries.⁹

The other idea was to utilize the auditory scaffolding hypothesis. This states that functions that include timing and processing are sent to the auditory system, which processes time-sensitive information. Cognitive functions require processing time-sensitive information and complex temporal organization. This is why scientists believe that listening to music can provide a scaffolding for either enhancing or relearning certain higher level functions such as speech. Since music is considered a complex temporal auditory language, it can enhance cognitive learning by using the auditory scaffolding model. After using this reasoning and conducting a study, researchers found that therapeutic music exercises do improve speech in patients who had a traumatic brain injury, strokes, and aphasia.⁹

IV. Limbic System

A. Anatomy & Physiology of the Limbic System

The final, but developing aspect of neurology that is affected by music therapy, is mood. The hippocampus and a structure known as the amygdala are a part of the limbic system which functions as a whole to process memories and manage emotional reactions. Specifically, music triggers emotional responses that are rapidly processed by various neural networks. If an emotion is correlated with a past memory, the neural networks that are activated will be different from a spontaneous response. The hippocampus serves a huge role in memory processing, specifically in sorting short-term memories from long-term memories. Since its main function is to process memories, any damage to the hippocampus will result in loss of memory, leading to degenerative memory disorders. Just as the limbic system associates emotions with past experiences, the hippocampus relies on life experiences to connect with music.⁹

Lastly, the amygdala controls response time to events, for example, the well-known fight-or-flight response. The amygdala sends a signal to the hypothalamus which then activates the sympathetic nervous system—a system of nerves that works in collaboration with the amygdala to carry out the fight-or-flight response. Since the amygdala is responsible for initiating spontaneous responses, it also connects memories with emotional encounters. If the amygdala were to experience any sort of damage, an individual would not be able to recognize emotion in music.⁸

B. Effects of Music on the Limbic System

When contrasting the emotion of music—sad or happy—the amygdala has an instantaneous reaction to the mood of music, perceiving it as either pleasant or depressing. This happens through the release of dopamine, a neurotransmitter that triggers feelings of joy. Because of this, an individual’s serotonin levels will also increase, thus decreasing negative emotions. By focusing on the melody and mood of the music, the limbic system is activated, stimulating several neural networks in the brain.³

C. Case Study on Patients with Autism

While mood is a rather unexplored field compared to cognition and movement, scientists have conducted several studies in order to prove their hypothesis. One of them was an Occupational Therapist who conducted a study with a group of children attending a specialized school for several disabilities, one of them being Autism. They attended a music therapy class three times a week, and they were clearly excited even before attending the class. In class, they experimented with singing songs, expressing emotions, and playing with several elements of music. After observing the children for a while, the therapist concluded that the students who had Autism, who once struggled with interaction, were now more social with their peers and teachers. Additionally, this motivated them to participate more not only in school, but also at home. This led to therapists believing that music therapy improved social skills and emotional intelligence in children with Autism, especially by altering elements of music such as mood and melodies.⁷

V. Conclusion

In conclusion, music therapy has been proven to be effective through its positive impact on degenerative neurological disorders. It has been found to affect three main sections of the brain: the cerebellum, frontal region, and the hippocampus. All three of these regions are drastically affected by neurological disorders ranging from dementia to traumatic brain injuries. In order to heal these particular areas, specific components of music were altered such as rhythm, timing, and mood. In order to determine this, several case studies were conducted and analyzed, all of which examined different neurological conditions. The first study investigated patients with Parkinson’s Disease and altered the rhythm production to form the conclusion that timing in a musical sentence would enhance neural networks, specifically in the cerebellum. Following that, a second study was conducted in order to determine the impact of specific music exercises on the frontal lobe. This led to the development of a complex hypothesis and ultimately proved the connection between music and an increase in cognitive functions. Lastly, the third study focused on children who were diagnosed with Autism. The purpose of this investigation was to explore the connection between mood, a relatively unexplored area, and the hippocampus. It was later determined that altering melodies in order to change the mood of the musical piece would improve social skills and increase emotional intelligence.

Because of the conclusions drawn from the case studies, scientists have laid the foundation for more creative forms of therapy that can potentially prove more effective than conventional therapy. By utilizing music as a therapeutic mechanism, patients are experiencing a drastic increase in neurological functions that they once lacked. Currently, music therapy is not a widespread practice, however, by emphasizing its positive impacts, scientists have the ability to help more patients and even extend this practice to neurological disorders.

However, while this review paper proved that music therapy is an effective practice for patients diagnosed with degenerative disorders, there were certain factors that were not considered. One of these limitations is neuroplasticity, or the brain’s ability to morph its structure in response to external stimuli. Music is considered an external stimulus, and it has been known to alter structures of the brain. However, the field is still developing. Scientists are unsure about the specific role neuroplasticity plays in cognitive functions as well as the involvement of words in music. Additionally, the frontiers of mood are endless and most of it has not been explored yet. Researchers are currently exploring the specific nature of emotional responses. Although they have been attempting to predict these responses, their data has been inconsistent because of its ever-changing nature. Furthermore, while the argument made in the paper regarding emotion heavily relies on music affecting an individual’s life experience, scientists still do not exactly know the correlation between the limbic system and how it processes previous occurrences. Lastly, scientists are currently wondering if music therapy can heal an individual’s brain, especially through the induction of mood. This area is quite unknown and inducing false emotions presents several constraints. Doing further research could eventually break the barrier surrounding conventional therapy, introducing more alternatives to our society.

References

[1] Barrett, L. F. (2021, March 3). That is not how your brain works. Nautilus. Retrieved October 7, 2022, from https://nautil.us/that-is-not how-your-brain-works-238138/

[2] Magee, W. L., & Stewart, L. (1AD, January 1). The challenges and benefits of a genuine partnership between music therapy and Neuroscience: A dialog between scientist and therapist. Frontiers. Retrieved October 7, 2022, from https://www.frontiersin.org/articles/10.3389/fnhum.2015.00 223/full

[3] Trimble, M., & Hesdorffer, D. (2017, May 1). Music and the brain: The neuroscience of music and musical appreciation. BJPsych international. Retrieved October 7, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5618809/

[4] Brain anatomy and how the brain works. Johns Hopkins Medicine. (2021, July 14). Retrieved October 7, 2022, from https://www.hopkinsmedicine.org/health/conditionsanddiseases/anatomy-of-the-brain

[5] Hamilton, J. (2022, February 19). Art and music therapy seem to help with brain disorders. scientists want to know why. News. Retrieved October 7, 2022, from https://www.wgbh.org/news/national news/2022/02/19/artand-music-therapy-seem-to-help-with-brain disordersscientists-want-to-know-why

[6] Steinhoff, N., Heine, A. M., Vogl, J., Weiss, K., Aschraf, A., Hajek, P., Schnider, P., & Tucek, G. (2015, August 21). A pilot study into the effects of music therapy on different areas of the brain of individuals with unresponsive wakefulness syndrome. Frontiers in neuroscience. Retrieved October 7, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4543917/

[7] Music and understanding emotions in children with autism. SOUNDSORY. (2021, April 13). Retrieved October 7, 2022, from https://soundsory.com/music-andunderstanding-emotions-in-children with-autism/

[8] Google. (n.d.). Music therapy handbook. Google Books. Retrieved October 7, 2022, from https://books.google.com/books id=mfnhBQAAQBAJ&printsec=frontcover#v=onepage&q&f=false

[9] Sashitzky, I. (2020, May 6). How music helps to heal the injured brain. Dana Foundation. Retrieved October 7, 2022, from https://dana.org/article/how-music-helps-to-heal theinjuredbrain/#:~:text=Biomedical%20researchers%20have%20found%20that,and%20reeducate%20the%20injured%20brain.

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The Minds of Serial Killers

Serial killers (individuals who murder multiple others and tend to have break or a “cool-off” period within their murders), and their stories constantly spur fascination among the public. But what do contemporary psychology and neuroscience have to say regarding what might be going on in these people’s heads? 

A common trait of serial killers is their lack of compassion for other people and their apparent lack of conscience. Nevertheless, a lot of people have a talent for appearing attractive on the surface, which enables them to draw unsuspecting others into their network of devastation. One explanation for this intellectual dishonesty is that serial killers have two minds at once. One is a rational self that can successfully navigate the complexities of acceptable social behavior and even charm and seduce, and the other is a much more sinister self that is capable of the most heinous and violent acts against others. However, on the contrary, there is very little evidence that serial killers do actually suffer from D.I.D. (Dissociative identity disorder), where people suffer from having two or more personalities co-existing in their mind, completely being nonchalant to one another. Instead, abuse victims who develop many identities as a coping mechanism for the traumas they have experienced are more likely to have DID than abusers. Of course, abusers can also be victims, and many serial killers suffered abuse as children, but generally speaking, these criminals don’t seem to have many personalities; rather, they seem to be mindful of the actions they are committing. Even so, there is undoubtedly a conflict in such people’s minds, which is perhaps best exemplified by US murderer Ted Bundy, who was “a charming, handsome, successful individual [yet also] a sadist, necrophile, rapist, and murderer with zero remorse who took pride in his ability to successfully kill and evade capture.”

One perplexing element of serial killers’ minds is that they don’t seem to have—or have the ability to suppress—the emotional responses that in other individuals help us recognize and empathize with the agony and suffering of other people. A new brain imaging research revealed a potential cause for this deficiency. The amygdala, a part of the brain that absorbs negative emotion and those that cause scared reactions, and the prefrontal cortex, which analyzes amygdala responses, had less connection in criminal psychopaths. When there is poor connection between these two areas, the amygdala’s processing of unpleasant stimuli does not result in any strongly felt unpleasant emotions. This could help to explain why criminal psychopaths do not experience guilt from their actions, or even pity their victims. Serial killers also appear to have an increased emotional drive that motivates them to want to harm and kill other people. The apparent discrepancy in emotional responses still has to be neurologically explained. Nevertheless, we shouldn’t exclude societal effects as significant contributors to the emergence of such conflicting drives. It appears plausible that serial killers have acquired the ability to regard their victims as little more than objects to be abused or perhaps even as a collection of unrelated pieces. This may help to explain why certain killers engage in sexual activity with their deceased victims or even use their corpses as ornaments or useful objects, but it does not help to explain why they appear to be so motivated to harm and kill their victims. The latter tendency can be explained by the fact that many serial killers are insecure people who are driven to kill out of a neurotic dread of rejection. The fear of rejection appears to frequently be brought on by having been neglected or abused by a parent. A young serial murderer could feel driven by such anxiety to want to kill anyone they have feelings for. They could start to think that they might avoid being deserted, humiliated, or otherwise injured as they were as children by eliminating the person they desire.

Additionally, serial killers seem to have no social conscience. We learn to identify good from wrong from our parents, siblings, teachers, peers, and other influential people as we grow up. This is what prevents us from acting in an antisocial manner. Serial killers, though, seem to believe they are above the most fundamental societal rule of them all—never taking another person’s life.

Aamu Yalamanchili, Youth Medical Journal 2022

Brain Organoids: A Narrative Review of Potential, Limitations and Future

Introduction

The rapid development of stem cell technology has opened up unprecedented avenues for studying human neurodevelopment. One of such avenue is the study of brain organoids, or “mini-brains”. These are three-dimensional, stem-cell derived suspension cultures, capable of self-assembling into organized forms with features resembling the human brain. 

While considerable progress has been made for in vitro models of organoid development for other systems—namely the intestine, pituitary and retina—three-dimensional culture modelling of the brain had for long remained out of reach, until a breakthrough study in 2013. In this study, led by postdoctoral student Madeline Lancaster, researchers developed innovative new methods to generate “cerebral” organoids, inspired by past work in the field with a focus on improving conditions for growth and higher-level development of cells. ‘Organoids’, in this sense, refer to stem-cell-derived, three-dimensional cultures that self organize to some extent and include multiple cell types and features of a particular organ. These developing tissues were placed in a rotational bioreactor. Within a few weeks, they yielded organoids containing anatomical brain structures resembling those of a 9-week-old human foetus. In the years since, developments in the field of stem cell research has allowed for other teams of researchers to give cerebral organoids increased degrees of structural complexity: from transplanting small organoids into mice to expose them to a greater supply of blood vessels, to making several organoids that mimic various parts of the brain and combining them for more complex cytoarchitecture. This provides immense potential for the study of human foetal brain development, neurodevelopmental disorders and degenerative diseases. 

However, it remains unclear precisely what cell types arise in these brain ‘organoids’, how much individual organoids vary, and whether mature neuronal networks can form and function in organoids. Many limitations and hurdles lie in the way of growth for this novel field, and even further, ethical questions await on the question of sentience and autonomy.

Technical Advances and Methodology 

To make an organoid in 2013, Lancaster’s team began with an embryoid body, floating aggregates of cells that resemble embryos. These could be obtained either from natural, embryonic stem cells (from the inner cell mass of a blastocyst) or from induced pluripotent cells, which were made from adult cells (typically skin cells) that would have been treated with four crucial biochemical factors which caused them to be reprogrammed to forego their original function and behave like embryonic cells. (See: Fig. 1) These embryoid bodies were differentiated into neural tissue and then transferred into three-dimensional gel matrix droplets. Once these ‘aggregates’ had reached a certain size, they were placed in a rotational bioreactor where they were spun to enhance to flow of nutrients into the medium without being shaped by the constraint of a vessel such as a Petri dish. 

With minimal external interference, this approach produced cerebral organoids possessing human pluripotent stem cells with the most freedom in regards to self-organisation and construction, exhibiting a variety of cell lineage identities, ranging from the forebrain, midbrain and hindbrain, to the retina, choroid plexus and mesoderm. 

This is known as the ‘unguided approach’ for the production of cerebral organoids. Although cell-type diversity offers a unique opportunity to model interactions between different regions of the brain, the high degree of variability and unpredictability present significant challenge for reproducibility and systemic studies.

On the other hand, in the ‘guided’ or ‘directed’ method for generating brain organoids, small molecules and growth factors are applied to developing organoids throughout the differentiation process to instruct human pluripotent stem cells to form cells and tissues resembling certain regions. These directed organoid cultures are sometimes capable of generating mixtures of cell types with relatively consistent proportions with less variation. However, they typically contain relatively small neuroepithelial structures and their architecture is often not well-defined. Nevertheless, the guided method remains the most common one for generating brain organoids today. 

There is also the avenue of advanced techniques that allow for greater complexity. This includes used organoid technologies, in which pluripotent stem cells are differentiated into region-specific organoids separately and then fused together, forming an end result with multiple distinct regional identities in a controlled manner. An example would be fused dorsal and ventral forebrain organoids, together forming an ‘assembloid’. These structures reveal the manner in which migrating interneurons connect and form microunits. 

The choice between guided and unguided methodologies will be dependent on the focus of the investigation. Where unguided organoids are suitable for exploring cell-type diversity during whole-brain development, brain region-specific organoids better mimic brain cytoarchitecture with less heterogeneity, and assembloids allow for the investigation of interactions between different brain regions.

With there being many routes to obtaining organoids that can then proceed to act as ‘models’, the logical next step in their development is their capability to, in fact, model the brain and study it, and what new avenues of treatment and application this can lead to.  

Potential Application 

As the organoids contain striking architectures strongly reminiscent of the developing human cerebral cortex (evolutionarily the most complex tissue), they display great potential for the effective modelling of neurodevelopmental brain disorders. As it would in the native brain, the cortical areas segregate into different layers, with radial glial cells dividing and giving birth to neurons in the innermost and subventricular zones, from which the quantity of neurons to develop the larger cerebral cortex is generated. 

This process presents fascinating opportunities for the study and treatment of microcephaly in particular. Microcephaly is a developmental conditions in which the brain of young infants remains undersized, producing a small head and debilitation. Replicating the condition is not suitable for mice models, as they lack the developmental stages for an enlarged cerebral cortex possessed by primates such as humans. Naturally, this means the disease would be impossible to show in a mouse model, as they do not have the developmental stage in which microcephaly is expressed in the first place. In this instance, brain organoids provide the most ideal model for study. 

Other studies involving brain organoids have been able to provide glimpses into the cellular and molecular mechanisms involved in brain development. For example, forebrain organoids derived from cells of individuals with ASD (autism spectrum disorders) display an imbalance of excitatory neuron and inhibitory neuron proportions. They have also developed great interest as potential neurodegenerative diseases models, even though attempts so far have had minimal success. This is mainly due to the fact that many neurodegenerative diseases, such as Alzheimer’s, are age-related and late onset, therefore brain organoids with mimic embryonic brain development may not possess the ideal characteristics to reproduce such development. 

In addition to genetic disorders, brain organoids can also provide models for neurotrophic pathogens such as the Zika virus. When brain organoids are exposed to the Zika virus, it results in preferential infection of neural progenitor cells (which suppress proliferation and cause an increase in cell death) leading to what is ultimately drastically reduced organoid size. They then also display a series of other characteristics identified in congenital Zika syndrome, such as the thinning of the neuronal layer, disruption of apical surface junctions and the dilation of the ventricular lumens. This highlights direct evidence of the causal relationship between exposure to the Zika virus and the development of harmful neurological conditions. In this way and many others, brain organoids provide optimistic prospects for the study of various neurodevelopmental diseases—though not without some considerations. 

Limitations

The fundamental limiting factor that prevents organoids from being able to fully replicate the late stages of human brain development is their size. Cortical organoids are much smaller in size compared with the full human cerebral cortex. Whereas cortical organoids can at most expand to approximately 4mm in diameter containing 2-3 million cells (about the size of a lentil), the human neocortex is about 15cm in diameter, with the thickness of gray matter alone being 2-4mm. This is a difference of about 50,000 in order. Furthermore, owing to a lack of circulation due to the limited metabolic supply, lack of a circulatory system and the physical distance over which oxygen and nutrients must diffuse, the viable thickness of organoids is restricted.  

Notably, cortical folding (gyrification) remains an unachieved ‘holy grail’ for cortical organoids. Gyrification is an essential and unique stage in the development of the human cortical brain in which the cerebral cortex experiences rapid growth and expansion. Due to the stressed of spatial confinement, the cortical layer buckles into wave-like structures, with outward ridges known as gyri and inward furrows called sulci. This stage is unique to humans and some other primates, theorised to be essential to complex behaviours such as language and social communication. In contrast, the brains of small such as rodents exhibit little to no gyrification—and neither do cerebral organoids. This may be because they are unable to reach the stage at which gyrification occurs (the demarcation of ‘primary’ gyri and ‘secondary’ gyri does not occur in humans until the second and third trimester, which is a later stage than what most brain organoids can replicate). Attempts have been made to induce ‘crinkling’ or ‘pseudo-folding’ in early organoid differentiation, but this has not led to the formation of gyrus- and sulcus- like structures. 

A better understanding of the mechanism under with gyrification occurs could lead to progress in existing methodologies to engineer the phenomenon in cerebral organoids, however, it is unlikely that the current organoid structure can fully replicate the folding of the human neocortex soon. Statistical analyses have suggested that the degree of folding across mammalian species is scaled with the surface area and thickness of the cortical plate, and organoids—at least in their current form—may simply be too small to achieve this result.

Due to these limitations, many ethical considerations concerning sentience and consciousness remain premature. The vast majority of scientists and ethicists are in agreement that consciousness has never been generated in a lab. Still, concerns over lab-grown brains have highlighted a blind spot: neuroscientists have no agreed upon definition or measurement of consciousness. Furthermore, certain experiments have still drawn scrutiny. In August 2019, a paper in Cell Stem Cell reported the creation of human brain organoids that produced co-ordinated waves of activity, resembling those seen in premature babies. While this was to a very small degree, it still prompted a wave of questions in relation to ethics, autonomy and ownership. Regardless, the waves only continued for a few months before the team shut the experiment down. Though moderate amounts of electrical activity is a sign of consciousness, the vast majority of brain organoids developed today are too far away in sophistication to be considered conscientious, autonomous beings.

Conclusion

Despite compelling data and innovative methodology, the formation of ‘a brain in a dish’ remains out of reach. Current models of brain organoids remain far from reproducing the complex, six-tiered architecture of their natural counterpart, even a foetal one. Presently, the organoids stop growing after a certain period of time and areas mimicking different brain regions are randomly distributed, often lacking the shape and spatial organisation seen in a sophisticated brain. Furthermore, there is also an absence of a necessary circulatory system means their interiors can often accumulate dead cells deprived of oxygen and nutrients. 

Yet, even with significant limitations, the potential for cerebral organoids are great. For certain questions, the model provided by this innovation could provide interesting answers and mechanism with which to study early human brain development and the progression of neurodevelopmental disorders. The brain organoid field has made exciting leaps to empower researchers and scientists with new tools to address old questions, and while there is a long path before more faithful in vitro representation of a developing human brain is reached, it is important to consider that no model will likely ever be perfect. 

Ishika Jha, Youth Medical Journal 2022

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The Neuroscience Behind Emotions: Exploring The Science Behind Emotions

Introduction

 Our daily lives are significantly impacted by our emotions. The emotions you encounter on a daily basis can spur you to action and have an effect on both major and minor life decisions. They can either be short-lived, or long-lasting. We make decisions based on how pleased, angry, depressed, bored, or dissatisfied we are. We choose activities and hobbies based on the feelings they elicit. Understanding these different types of emotions can help us navigate life more easily and steadily. (3). According to the Project on the decade of the brain: “The Science of Emotion”, emotions are a brief period of synchronized brain, autonomic, and behavioral changes that aid in responding to an event. They are a highly adaptable type of physiological response that governs our existence and are low-level responses that are encoded in our DNA. Emotion is mostly exhibited in the body’s theater, through posture and facial expression, as well as through internal processes such as heart rate and blood pressure. Feelings are high-level responses that provide a mental and perceptual representation of what is happening physiologically inside our bodies. 

What are Emotions? 

Authors Don Hockenbury and Sandra E. Hockenbury claimed in their book “Discovering Psychology” that an emotion is a complex psychological state with three separate components: a subjective experience, a physiological response, and a behavioral or expressive response. (4). In addition to attempting to explain what emotions are, scholars have attempted to identify and categorize the various sorts of emotions. Over time, the explanations and insights have evolved.

Emotions are reactions that people have in response to events or situations. The circumstance that causes the emotion determines the type of emotion the individual feels. There are four major emotions: happiness, sadness, fear, and anger, which are associated with three core affects: reward, punishment, and stress. The fundamental emotions are internal states that are controlled by neuromodulators. These internal states are expressed externally as certain stereotypical actions, such as instinct, which is thought to be one of the first means of survival. (2). According to the study on Drosophila and other insects, it states that emotion is essential in both regular human experience and psychiatric diseases. Despite the importance of emotion, the relative absence of objective approaches for scientifically examining emotional phenomena restricts our existing understanding and hence necessitates the creation of novel methodologies. To add on, using behavioral studies of Drosophila, they have created a theory of the fundamental emotions. Basic emotions are internal states generated by fundamental physical changes, which can then lead to genetically “hardwired” innate responses. They have been substantially preserved throughout evolution and share key functional and adaptive features across a broad phylogenetic range.

How do emotions work?

Our brain is covered in neural networks that become stronger or weaker as they are used. Those that are utilized repeatedly form very strong ‘neural highways,’ defining our default thinking, emotional profile, and personality. The good news is that neuroplasticity, the ability to modify brain connections, exists. (5). The interoceptive network in the brain constantly monitors your bodily sensations, such as your heartbeat, lungs filling and emptying, intestines operating, and stomach (slightly) aching. Your brain (encased in its dark, quiet cage known as the skull) attempts to decipher what these physiological feelings signify based on both information received from the outside world via your senses and past experience. (6). Each emotion has a distinct location in the brain. 

Three brain areas appear to be most closely associated with emotions: the amygdala, the insula or insular cortex, and the periaqueductal gray tissue in the midbrain. 

The amygdala, a paired, almond-shaped structure deep within the brain, integrates emotions, emotional behavior, and motivation. It interprets fear, distinguishes friends from opponents, and identifies social incentives and how to obtain them. The amygdala is also involved in classical conditioning, a sort of learning. According to Brainfacts: “The Anatomy of Emotions”, they talk about Russian biologist Ivan Pavlov, who in his experiments on digestion in dogs, initially described classical conditioning, in which a stimulus evokes a certain response through repeated exposure. When a lab technician offered them food, the dogs salivated. Over time, Pavlov saw that even when the technician was empty-handed, the dogs would start to salivate at his sheer presence. 

The insula is the source of distaste — a strong negative reaction to an unpleasant odor, for example. The sensation of revulsion may keep you from consuming poison or damaged food. When someone feels or expects pain, the insula lights up with activity, according to studies utilizing magnetic resonance imaging (MRI). According to neuroscientists, the insula receives a status report on the body’s physiological state and develops subjective feelings about it, hence connecting internal states, feelings, and conscious actions.

The periaqueductal gray, which is found in the brainstem, has also been linked to pain perception. It has receptors for pain-relieving substances such as morphine and oxycodone, and it can assist quiet activity in pain-sensing nerves, which may explain why you can occasionally distract yourself from pain so you don’t experience it as keenly. In addition to protective and reproductive activities, maternal bonding, and anxiety, the periaqueductal gray is involved in anxiety.

Together, these different parts of the brain, including the central and peripheral nervous system make up our vast sense of emotions.

How do emotions influence our daily life?

If you were asked what makes you human, emotions – or some component of your personality that is closely tied to emotions – could be near the top of the list. Our emotions have an impact on our relationships, our career, our lifestyle, our sense of ourselves, and our large and small decisions. Darwin was captivated by emotions and came to the conclusion that they exist to alert us quickly whether a situation is safe. Wrecognize the significance of our emotions in this and many other ways. We are aware that anger may be a source of strength, love keeps us connected to other people, and fear encourages us to cross the street carefully. However, we frequently have a tangled connection with our emotions, labeling some as positive and others as harmful. We may conceal and dismiss those we don’t want or consider ‘acceptable,’ while pursuing those we do, potentially to our cost. However, we frequently have a tangled connection with our emotions, labeling some as positive and others as harmful. We may conceal and dismiss those we don’t want or consider ‘acceptable,’ while pursuing those we do, potentially to our cost. Overall our emotions have a big influence on how we live our daily lives. You can be motivated to take action and have an impact on both major and minor life decisions by the feelings you encounter every day.

Akshaya Ganji, Youth Medical Journal 2022

References

1. Project on the decade of the brain: “The Science of Emotion”-https://www.loc.gov/loc/brain/emotion/Damasio.html 
2. Frontiers: “A Model for Basic Emotions Using Observations of Behavior in Drosophila”-https://www.frontiersin.org/articles/10.3389/fpsyg.2019.00781/full 
3. Verywellmind: “Emotions and Types of Emotional Responses (The Three Key Elements That Make Up Emotion)”-https://www.verywellmind.com/what-are-emotions-2795178 
4. Hockenbury D. Hockenbury SE. Discovering Psychology. Worth Publishers 
5. Welldoing: “The Neuroscience of Emotions”- https://welldoing.org/article/neuroscience-emotions 
6. Behavioral Research Blog: “How emotions are made” –https://www.noldus.com/blog/how-emotions-are-made 
7. Brainfacts: “The Anatomy of Emotions”-https://www.brainfacts.org/thinking-sensing-and-behaving/emotions-stress-and-anxiety/2018/the-anatomy-of-emotions-090618 

The Science Behind Déjà Vu

Have you ever looked at something and have had an eerie thought of familiarity? “Wait, I feel like I have already been here before..”, “This is so weird, I swear I met you somewhere..”, or even something as simple as, “I felt like I already bought the groceries for this week.” So, what is this feeling? Will science be able to explain it? 

Carrie-Ann Moss, as “trinity in the matrix trilogy”, describes déjà vu as “a glitch in the matrix”. Is it really? Does this mean we, as humans, live in a simulation? Are we a video game? What even is this? This explanation is perfect for those late night thoughts and science fiction fans, as it doesn’t give a solid understanding of what it actually is! The sensation of déjà vu is brief and frequently unexpected, which is why we equate it with mystery and even the otherworldly. déjà vu intrigues us for the same exact reasons that make studying difficult. This oddity occurs in about 60% of the population. Because it is a transient sensation and there isn’t a definite trigger for it, déjà vu is challenging to investigate in the lab. Nevertheless, depending on their proposed assumptions, academics have employed a variety of methods to explore the phenomenon. Researchers may conduct participant surveys, research potentially associated processes, particularly those connected to memory, or develop additional experiments to test the phenomenon of déjà vu.

Regarding memory, most of the explanations surrounding this theory are built off the idea that you have experienced a situation in the past, or something very similar to it. You remember this situation with your unconscious mind, but forget it through your conscious mind. Therefore, giving that feeling of familiarity even though you don’t know why. For example, the single element familiarity hypothesis. The single element familiarity hypothesis proposes that if one aspect of the situation is familiar to you but you aren’t cognizant of it since it’s in a different location, such as if you see your doctor on the street, you will feel a sense of déjà vu. Even if you don’t recognize your doctor, your brain still associates that sensation of familiarity with the entire setting. This theory has also been expanded by other academics to include several components. The gestalt familiarity hypothesis concentrates on the arrangement of objects in a scene and how déjà vu happens when you see something with a similar layout. For instance, even if you haven’t seen your friend’s sofa in their living room previously, you may have seen a room with the same sofa in a different house. Having no memory of the other house, you have a sense of déjà vu. The gestalt similarity hypothesis has the benefit of being more easily verified. In one study, participants viewed virtual reality images of rooms before being asked how familiar a new space seemed and whether they felt like they were having déjà vu.  The researchers discovered that when the new room resembled the old ones, study participants who couldn’t remember the old ones tended to assume it was familiar and that they were having déjà vu. Additionally, these scores were higher the more similar the new space was to the old room.

According to some theories, déjà vu occurs when there is spontaneous brain activity unrelated to the current situation. You may experience a false sense of familiarity if that occurs in the area of your brain responsible for remembering. Some of the data comes from people who have temporal lobe epilepsy, which is characterized by aberrant electrical activity in the area of the brain that controls memory. These patients may have déjà vu when their brains are electronically stimulated as part of a pre-surgery examination. According to one study, déjà vu occurs when the parahippocampal system, which aids in recognizing familiar objects, inadvertently malfunctions and leads you to mistakenly believe that something is familiar when it isn’t. Others have argued that déjà vu cannot be attributed to a single system of familiarity, but rather incorporates a variety of memory structures as well as the relationships among them. 

Other theories are based on the speed at which information moves through the brain. Your brain’s many “lower order” areas send information to “higher order” areas, which combine data to help you make sense of the outside world. Your brain perceives your environment inaccurately if this intricate process is somehow interfered with—for example, if one component delivers something slower or faster than usual.

Despite the fact that all of the aforementioned theories seem to share one element in common, an explanation for déjà vu has yet to be found. In order to be more certain of the proper explanation, scientists might continue to create tests that more directly examine the nature of déjà vu.

Aamuktha Yalamanchili , Youth Medical Journal 2022

References

https://www.scientificamerican.com/article/can-science-explain-deja-vu/

https://www.sciencefocus.com/the-human-body/deja-vu/

https://www.bustle.com/wellness/how-does-deja-vu-work-theres-a-scientific-explanation-for-this-bizarre-phenomenon-2920454

https://www.discovermagazine.com/mind/whats-really-happening-when-you-experience-deja-vu

Anxiety Disorder: Exploring The Reality Behind Having Anxiety

Anxiety. A term that is used so frequently that it lost its meaning. This article covers the biology of the illness, how it is processed in the brain, its influences on individuals and the various diagnosis and treatment. 

Introduction

Experiencing anxiety or feeling anxiousness is a part of life. However, people suffering from anxiety disorders usually experience severe, excessive, and persistent worry and fear about ordinary events. These uncomfortable, hard to regulate, out-of-proportion to the real threat, and protracted sensations of worry and panic interfere with daily activities. According to the American Psychiatric Association entitled “What are Anxiety Disorders?” (1),  Anxiety is a typical response to stress and in some circumstances, it can be beneficial. It can alert us about potential threats and assist with planning and attention. Anxiety disorders are distinguished from typical sensations of nervousness or anxiety by the presence of excessive fear or anxiety. According to the Nami National Alliance on Mental Illness, titled, “Anxiety Disorders”(2),  they stated that “ Anxiety disorders are the most common type of mental illness in the United States. In the US, approximately 40 million persons (19.1%) suffer from an anxiety illness. Meanwhile, approximately 7% of children aged 3-17 experience issues with anxiety each year, and most people develop symptoms before age 21.”

 To add on, there are 5 major types of Anxiety. Generalized Anxiety Disorder, Obsessive-Compulsive Disorder (OCD), Panic Disorder, Post-Traumatic Stress Disorder (PTSD), and Social Phobia (or Social Anxiety Disorder). 

What causes Anxiety Disorder?

Having Anxiety Disorder interferes with daily activities and is difficult to control. And so, what is the cause? The specific cause of anxiety disorders is unknown to researchers. Although, throughout examination, researchers have found that there are various causes of Anxiety Disorder, and each is based on its different types. 

It can be caused by genetics, since Anxiety Disorders may run in families. There could be environmental stress, such as childhood abuse and neglect, the death of a loved one, and several other traumatic situations. Anxiety Disorders can be caused with drug abuse or withdrawal. Some anxiety symptoms may be concealed or reduced with specific medications, and so alcohol and drug abuse can go hand in hand with anxiety disorders. Some heart, lung, and thyroid diseases can exacerbate or induce symptoms that are similar to those of anxiety disorders. (4)

According to several studies, dysfunctional brain circuits that regulate emotions and fear may be responsible for anxiety disorders. They are characterized by a variety of neuroendocrine, neurotransmitters, and neuroanatomical abnormalities. The great degree of interconnectedness between neurotransmitter- and neuropeptide-containing circuits in limbic, brain stem, and higher cortical brain areas complicates identifying the most functionally significant differences. Additionally, environmental events and underlying genetic predisposition may lead to a primary alteration in brain structure or function or in neurotransmitter signaling; such abnormalities might raise the risk for psychopathology. (3)

To continue, it’s important to consider the neurotransmitters that allow communication between different regions. When there is an increased activity in the limbic system and various emotion-processing brain regions, patients who have Anxiety Disorder could have a decrease in inhibitory signals by by γ-amino-butyric-acid (GABA) or increased excitatory neurotransmission by glutamate. Each anxiety disorder, as well as major depressive disorder (MDD), is vulnerable due to both genetic and environmental factors.

Overall, Anxiety is produced by an imbalance in the brain chemicals serotonin and noradrenaline, which are important in mood regulation; a combination of past trauma such as assault, abuse, or bullying; chronic pain condition; or inherited causes, among other things. The decision to identify MDD, PD, PTSD, SAD, and GAD as different illnesses must be established on pathophysiology, genetics, duration of illness, and treatment response data, in addition to clinical phenomenology. The variations in neuroendocrine, neurotransmitter, and neuroanatomical functions between individuals with mood or anxiety disorders and healthy control subjects must be evaluated with caution (Table 3). Brain areas and neurotransmitter systems associated in mood and anxiety disorders perform a variety of activities, many of which are unrelated to the etiology of psychiatric diseases. (3)

Figure 1: Pearson: “Structures under the Cortex: The Limbic 

System”

Figure 2: National Library of Medicine: “The Neurobiology of Anxiety Disorders: Brain Imaging, Genetics, and Psychoneuroendocrinology.”

Symptoms of Anxiety

The primary symptoms of Anxiety prevail of 

• panic
• uneasiness
• hyperventilation
•  tense muscles
•  rumination
• fervently avoiding dreaded things or locations
• Having an increased heart rate
• Sweating
• Feeling weak 
• difficulty focusing or thinking about anything but the current issue 
• Having digestive issues 
• having trouble managing worry 
• a desire to stay away from things that make you anxious

How Anxiety affects individuals

An anxiety-inducing scenario or impending event is a typical physical response to stress. This reaction starts in the Amygdala, a part of the brain that sends distress signals to the hypothalamus. (Fig 1).  The remainder of the body receives these signals, which triggers a “fight or flight” reaction. A short-term, physiologically positive stress reaction occurs when the adrenaline hormone, an elevated heart rate, increased blood supply to the brain, and the ensuing surge of oxygen compel us to focus on the issue and find a solution. However, long-term repetitive stress reactions to anxiety, excessive worry, and a variety of day-to-day concerns. There are 5 major types of Anxiety and each type affects the individual differently.

Generalised Anxiety Disorder (GAD)

With GAD, you experience excessive, unreasonable tension and concern for little to no reason. You worry excessively about most everyday circumstances and can’t recall the last time you felt calm and collected. This constant stress and tension may be accompanied by bodily symptoms such as restlessness, feeling on edge or quickly fatigued, difficulties concentrating, muscle strain, or sleeping issues. Worries about ordinary things such as job duties, family health, or minor issues such as chores, car maintenance, or appointments are common. (1)

Obsessive-Compulsive Disorder (OCD)

OCD can induce obsessive, intrusive thoughts that can be stressful, as well as an overpowering desire or compulsion to execute a routine repeatedly. This could be shown in his or her behaviors, such as cleaning or washing hands excessively, putting goods in a drawer in a specific way, folding away clothes, and so on. (5)

Panic Disorder

Panic Disorder involves recurrent episodes of abrupt, severe feelings of worry, fear, or terror that peak in just a few minutes (panic attacks). You might experience dread, breathlessness, chest pain, or a rapid, fluttering, or hammering heart (heart palpitations). These episodes don’t coincide with a recognized phobia or stressor; instead, they happen “out of the blue.” (7), and so these panic attacks might lead you to worry about them happening again or to avoid circumstances where they have happened.

Post-Traumatic Stress Disorder (PTSD)

PTSD is a psychiatric disease that can arise in people who have encountered or witnessed a traumatic event such as a natural catastrophe, a catastrophic accident, a terrorist attack, war/combat, or rape, or who have been threatened with death, sexual violence, or serious injury. People suffering from PTSD have powerful, unsettling thoughts and sensations about their experience that remain long after the traumatic event has finished. They may relive the event in flashbacks or dreams, experience sadness, dread, or fury, and feel disconnected or estranged from others. Persons suffering from PTSD may avoid circumstances or people that remind them of the traumatic experience, and they may have significant unpleasant reactions to seemingly innocuous things such as a loud noise or an unintentional touch. (6)

A traumatic incident must have occurred in order for PTSD to be diagnosed. The exposure, however, may be indirect rather than direct. A person who sees the violent death of a close family member or friend, for example, may develop PTSD. Some of the many symptoms and diagnosis of PTSD include Intrusive thoughts, resisting reminders of the traumatic event, changes in cognition and personality, and changes in arousal and reactivity. (6)

Social Phobia (Social Anxiety Disorder)

Social anxiety disorder (social phobia) is characterized by intense anxiety, fear, and avoidance of social interactions as a result of emotions of humiliation, self-consciousness, and concern about being judged or seen adversely by others.

Risk factors

Anxiety disorders are caused by a variety of reasons, including genetic, environmental, psychological, and developmental factors. Anxiety disorders can run in families, implying that the diseases are caused by a mix of genes and environmental factors. (1). A few factors are, 

• Truma
• Stress from an illness
• Other mental health disorders 
• Drug or alcohol 
• And many others.

Diagnosis and Treatment

The first step is to see your doctor to ensure that there is no physical problem causing the symptoms. If you are diagnosed with an anxiety disorder, a mental health expert can help you find the appropriate treatment. Unfortunately, many people suffering from anxiety problems do not seek treatment; they are usually unaware that they are suffering from a disease. Although each anxiety condition is distinct, the majority respond effectively to two methods of treatment: psychotherapy (often known as “talk therapy”) and medicines. These treatments can be administered individually or in combination. 

Psychotherapy, often known as talk therapy or psychological counseling, entails working with a therapist to minimize your anxiety symptoms. It might work well as an anxiety therapy. 

The most effective type of psychotherapy for anxiety problems is cognitive behavioral therapy (CBT). CBT is a short-term treatment that focuses on teaching you how to think, react, and behave differently in order to feel less nervous. There are particular strategies to help you improve your symptoms and gradually return to the activities you’ve avoided due to anxiety. 

CBT incorporates exposure treatment, in which you gradually expose yourself to the object or event that causes your anxiety in order to gain confidence in your ability to manage the situation and anxiety symptoms. (8)

 Although medications will not cure anxiety disorders, depending on the type of anxiety disorder you have and whether you also have other physical or mental health problems, they can provide significant relief from symptoms. The most often given drugs are antidepressants and anti-anxiety meds, which are typically only provided temporarily.

In some cases, your doctor may prescribe other medications, such as sedatives, often known as benzodiazepines, or beta-blockers, which are commonly used to treat cardiac issues, are also used to treat physical symptoms of anxiety. These drugs are meant for short-term alleviation of anxiety symptoms and should not be used indefinitely. (8)

Self-Help, Coping, and Managing

People can also do a variety of things to help cope with the symptoms of anxiety disorders and make treatment more successful. Meditation and stress-reduction methods can be beneficial. They can join support groups (in person or online) that can allow people to share their experiences and coping mechanisms. They can learn more about the nuances of a disorder and assist family and friends in better understanding the condition can also be beneficial. To include, caffeine, which can aggravate symptoms, should be avoided, and any drugs should be discussed with your doctor.

Akshaya Ganji, Youth Medical Journal 2022

 References 

1. American Psychiatric Association: “What are Anxiety Disorders?”-https://psychiatry.org/patients-families/anxiety-disorders/what-are-anxiety-disorders. 
2. Nami National Alliance on Mental Illness: “Anxiety Disorders”-https://www.nami.org/About-Mental-Illness/Mental-Health-Conditions/Anxiety-Disorders 
3. National Library of Medicine: “The Neurobiology of Anxiety Disorders: Brain Imaging, Genetics, and Psychoneuroendocrinology.”-https://www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc-20350961 
4. WbMD: “Anxiety Disorders”-https://www.webmd.com/anxiety-panic/guide/anxiety-disorders 
5. MayoClinic: “Anxiety Disorders”-https://www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc-20350961 
6. American Psychiatric Association: “What is Posttraumatic Stress Disorder (PTSD)?”-https://psychiatry.org/patients-families/ptsd/what-is-ptsd 
7. National Institute of Mental Health: “Panic Disorder”-https://www.nimh.nih.gov/health/statistics/panic-disorder 
8. MayoClinic: “Anxiety Disorders (Dignonis)-https://www.mayoclinic.org/diseases-conditions/anxiety/diagnosis-treatment/drc-20350967 

The Neurobiology and Superficial Traits of Psychopathy

Introduction

The word ‘psychopath’ can often be used as a throw-away term to describe someone violent and cruel, but this a minimised view on the disorder. Additionally, psychopathy tends to be confused with sociopathy – but in an interview with the psychologist Ramani Durvasula, PhD, she says “the key difference: a psychopath is born, and a sociopath is made.” (2). While psychopathy does have environmental factors, it also has a strong genetic component  – but interestingly, individuals can be genetically predisposed to having psychopathy, yet the disorder remains dormant unless exacerbated by external factors. However, psychopathy is more common than typically believed – as it is estimated to affect 1% of the global population and is observed to be more prevalent in men than women. Interestingly enough, psychopathy affects between 15 and 25% of the prison population worldwide, thus implying an association between mental illness and criminality (3).

Psychopathic Traits

Psychopathy is characterised by various personality traits and behaviours, especially a lack of empathy, impulsivity, pathological lying, manipulative behaviour, and high intelligence (1). The reduced empathetic response is considered to be the most common psychopathic trait and can be observed through a willingness to engage in anti-social behaviour, a disregard for the impacts of their actions on other people, and a decreased physiological response to emotional stimuli (3). The latter is believed to be due to hyporeactivity of the autonomic nervous system to stimuli in psychopathic individuals compared to non-psychopathic individuals. However, psychopathy in itself is not an ‘official’ psychiatric diagnosis, and instead the term Antisocial Personality Disorder is used instead.

(8)Further, psychopathy and sociopathy are frequently used interchangeably in the media and film especially – and while these conditions share similarities, there are several differences. The main connection between psychopathy and sociopathy is engagement in anti-social behaviour, for instance, physical violence, harassment, vandalism, and other more serious offences (9). Other key similarities include: aggression, deceitfulness, anti-social behaviour, irresponsibility, impulsivity, and a lack of remorse and guilt. As mentioned earlier, it is the consensus that psychopaths are born while sociopaths become so as a result of their environmental factors. Having difficulty forming emotional attachments is a common psychopathic trait, as well as appearing charming and trustworthy by others. As well, psychopaths tend to be more strategic when engaging in anti-social behaviour so as to minimise the risk to themselves – but have little or no feeling of guilt as to the repercussions of their actions for others. Sociopaths are generally more erratic than psychopaths, and act more impulsively. Like psychopaths, sociopaths can also struggle to form emotional attachments – but this is not the case for all.

The Neurobiology of Psychopathy

Psychopathy is also believed to be greatly associated with the amygdala, and it has been hypothesised that amygdalar changes could be a source of deficit processing of fear-related responses in psychopathic individuals (4). In an article entitled ‘Localization of deformations Within the Amygdala in Individuals With Psychopathy’ (5), research was carried out with the purpose to detect amygdalar anatomical abnormalities in psychopathic individuals. The study consisted of 27 individuals who were psychopathic, and their amygdalar volumes were determined using volumetric analysis and surface-based mesh modelling methods. This meant any regional surface abnormalities would be able to be detected. The results showed that the individuals with psychopathy had significantly lower bilateral volumes of the amygdala compared with the control group – 17.1% on the left and 18.9% on the right. As the amygdala is necessary to incite the feeling of fear and fear conditioning, abnormalities in this anatomical structure can explain a lack of fear conditioning and response to dangerous situations in psychopathic individuals. Moreover, another function of the amygdala is social interaction and moral reasoning – and when there are structural abnormalities in the amygdala, this can show why psychopaths can lack the ability to recognise emotions in others, as well as poor moral judgement. 

In addition, psychopathic individuals can present with dysfunction of the ventromedial prefrontal cortex (vmPFC), which can impair the function of emotion and emotion regulation (6). The neuroscientist Antonio Damasio carried out research to investigate the connection between damage to the vmPFC and various emotion and decision- making deficits. Associations were made between dysfunction of the vmPFC and diminished shame, guilt, and empathy, as well as irritability and irresponsibility. The findings of this study also showed that psychopaths and patients who had suffered damage to their vmPFC had reduced autonomic arousal to emotional stimuli – thus showing that there are neurological explanations behind the lack of fear and acknowledgement of consequence in psychopathic individuals.

Another region of the prefrontal cortex potentially involved in psychopathy is the anterior cingulate cortex (ACC). Activity in the ACC has been associated with functions such as pain, empathy, negative affect, and performance. Patients who had lesions of the ACC have been shown to often exhibited greater irritability than those without, in addition to social disinhibition (6).

The case of the railroad construction worker Phineas Gage in the 19^th Century (7) can further build on the link between the dysfunction of or injury to the prefrontal cortex and psychopathic traits. In a horrific accident at the railroad, Gage had an iron rod shot at his head – this had the effect of damaging his prefrontal cortex. Gage survived, but the most notable effect of this accident was the substantial changes in his personality; before he had been kind and dependable, but then became impulsive, rude, and disrespectful. These changes helped to identify the function of the prefrontal cortex, and these new personality traits that Gage had are very similar to those with psychopathy. After a number of similar cases during the 20^th Century with damage to the prefrontal cortex resulting in personality changes, the term ‘pseudopsychopathy’ was coined to describe this association.

Diagnosis of a Psychopath

An important diagnostic tool for psychopathy is the Hare psychopathy checklist, created by the psychologist Dr Robert Hare (11). This checklist has been revised and is now formally known as the Hare PCL-R (Hare Psychopathy Checklist – Revised). In the PCL-R, there is an interview and a review of the patient’s history as two separate parts. The PCL-R evaluates to what extent an individual fulfils twenty psychopathic traits, such as lacking remorse or guilt, and having a grandiose sense of self-worth; the figure below categorises all of the traits being examined. When the PCL-R has been completed, the individual will have a score between 0 and 40 – 0 means they have no psychopathic tendencies or traits, whereas the latter means they are the paragon of a psychopathy. For each of the twenty psychopathic traits that the individual demonstrates, they are given a score between 0 and 2, depending on how greatly it is applicable to them. If the individual has a score greater than 30, this means they are a psychopath – and so qualify for a diagnosis, though the diagnosis would be of Antisocial Personality Disorder. (10,12)

Case Studies of Psychopathic Traits and Individuals

Hervey Cleckley, M.D., was an American psychiatrist and arguably the most influential historical figure in the field of psychopathy(13). Cleckley researched psychopathy throughout his academic career and compiled 15 case studies of prototypic psychopaths in his novel ‘The Mask of Sanity’ (14). One of the case studies in this novel is that of Tom, who is described by Cleckley as being an intelligent and healthy young man whose family were hoping for him to be diagnosed with some psychiatric disorder so that he would not serve jail time for his stealing. Cleckley describes how Tom would often skip school – suggestive of the psychopathic traits of a need for stimulation and irresponsibility – and that he would frequently steal from his family – embodying the psychopathic trait of criminal versatility. Furthermore, as a child, Tom often partook in delinquent behaviour, including shoplifting, setting fire to a privy in his local area, and throwing rocks at squirrels in the park – and again, these poor behavioural problems from an early age are also listed as psychopathic attributes in the Hare Psychopathy Checklist (Revised). When he became a teenager, Tom’s behaviour worsened, and he escalated from petty theft to car stealing and breaking into homes. Additionally, Tom was described as lying pathologically and doing so with sufficient charm to be convincing. For the next several years up to the age of 21 when Cleckley met him, Tom spent frequent spans of time in prison for stealing, initiating fights and various other instances of anti-social behaviour. The other fourteen case studies discussed in his novel detail people exhibiting very similar behaviour and characteristics. In analysis of these cases, Cleckley wrote “some of these patients I believe are definitely psychopaths but to a milder degree”. However, Cleckley also wrote that a person who engaged in anti-social behaviour was not definitively a psychopath, and through his research and analysis of psychopathy he worked to compile ideas about psychopaths as specific individuals – such as ‘the psychopath as a gentleman’ and ‘the psychopath as a scientist’. Overall,‘The Mask of Sanity’ formed the basis of what is now known as ‘psychopathy’, and led to considerable development in the study of this condition.

Another example of case studies of psychopathy can be found in the article ‘Incurable Psychopaths?’ by Marianne Kristiansson, MD (15). The first case detailed in this article is one of a 38-year-old man, who exhibited hyperactivity, restlessness and had engaged in criminal behaviour for many years – and had 13 convictions, including for assault. He had a history of drug and alcohol abuse and was admitted for a forensic psychiatric evaluation after he was suspected of assault again. This man was examined using the Hare Psychopathy Checklist Revised (PCL-R) and scored 36. This resulted in him being diagnosed with antisocial personality disorder and was thereafter treated with lithium. This treatment method appeared to stabilise him and led to a drop in his criminal behaviour and restlessness. Modern day treatments for antisocial personality disorder, however, often do not involve medication but rely on therapy – such as cognitive behaviour therapy – instead. 

Conclusion

In the modern world, the term ‘psychopath’ tends to be used more in the legal sense – often in cases of forensic psychiatric evaluations of criminals – than in the medical sense, and this is why psychopathy has a stigma of being equated to violent criminality. While the two are not mutually exclusive, psychopaths can lead relatively normal lives without anyone, including themself, being aware that they are a psychopath. Arguably it is difficult to achieve this though, as psychopaths often lack the ability to form long-term emotional connections – and as a fundamental basis of human nature this can complexify and isolate their lives. Further, the previous diagnosis of psychopathy as antisocial personality was solely based on the superficial traits listed in the PCL-R, modern research into the neurobiology of this condition can make diagnosis more accurate. Moreover, it shows how being a psychopath is an innate condition rather than singularly the product of the environment in which the individual is surrounded by – and especially that the prefrontal cortex is the region of the brain most closely linked with psychopathy to date. Despite this progress, the quote from Cleckley’s ‘Mask of Sanity’ still stands: “I do not believe that the cause of the psychopath’s disorder has yet been discovered and demonstrated. Until we have more and better evidence than is at present available, let us admit the incompleteness of our knowledge and modestly pursue our inquiry.” (14).

Samara Macrae, Youth Medical Journal 2022

References

1.   Psychiatric Times: “The Hidden Suffering of the Psychopath” – https://www.psychiatrictimes.com/view/hidden-suffering-psychopath

2.   YouTube – MedCircle: “Narcissist, Psychopath, or Sociopath: How to Spot the Differences” – https://www.youtube.com/watch?v=6dv8zJiggBs

3.   Science Direct: “Psychophysiology of Mental Health” by B.F. O’Donnell, W.P Hetrick – https://www.sciencedirect.com/topics/neuroscience/psychopathy

4.   Journal of Young Investigators: “The Fear Factor: Fear Deficits in Psychopathy as an Index of Limbic Dysregulation” – https://www.jyi.org/2019-june/2019/6/1/the-fear-factor-fear-deficits-in-psychopathy-as-an-index-of-limbic-dysregulation

5.   Journal of the American Medical Association: “Localization of Deformations Within the Amygdala in Individuals With Psychopathy” – https://jamanetwork.com/journals/jamapsychiatry/article-abstract/210298

6.   US National Library of Medicine: “The role of prefrontal cortex in psychopathy” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3937069/

7.   Smithsonian Magazine: “Phineas Gage: Neuroscience’s Most Famous Patient” – https://www.smithsonianmag.com/history/phineas-gage-neurosciences-most-famous-patient-11390067/

8.   Mental Health America: “Psychopathy vs Sociopathy” – https://www.mha-em.org/im-looking-for/mental-health-knowledge-base/conditions/127-psychopathy-vs-sociopathy

9.   WDH: “Examples of antisocial behaviour”  –https://www.wdh.co.uk/OurCommunities/CommunitySafety/ExamplesOfAntisocialBehaviour/

10.   Encyclopaedia: “Hare Psychopathy Checklist” – http://www.minddisorders.com/Flu-Inv/Hare-Psychopathy-Checklist.html

11.   Wikipedia: “Robert D. Hare” – https://en.wikipedia.org/wiki/Robert_D._Hare

12.   The European Journal of Psychology Applied to Legal Context: “A contrastive analysis of the factorial structure of the PCL-R: Which model best fits the data?” –  https://www.elsevier.es/en-revista-the-european-journal-psychology-applied-381-articulo-a-contrastive-analysis-factorial-structure-S188918611400016X

13.   APA PsycNet: “Cleckley’s psychopaths: Revisited” – https://psycnet.apa.org/record/2015-53846-001

14.   ‘The Mask of Sanity’ by Hervey Cleckley, M.D. (5th edition) – https://www.gwern.net/docs/psychology/1941-cleckley-maskofsanity.pdf

15.   ‘ResearchGate: “Incurable Psychopaths?” by Marianne Kristiansson, MD – https://www.researchgate.net/profile/Marianne-Kristiansson/publication/14560546_Incurable_psychopaths/links/562a7e2f08ae518e347f54f1/Incurable-psychopaths.pdf

ADHD: Over Diagnosed or Loosely Defined?

Introduction

Attention deficit hyperactivity disorder (ADHD) is generally manifested through difficulty focusing. The disorder’s diagnostic criteria, as described in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), includes a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development, the presence of several inattentive or hyperactive-impulsive symptoms prior to the age of twelve and in two or more settings, clear evidence the symptoms interfere with social, academic, or occupational functioning, and the precedent that the symptoms cannot be explained by another mental disorder. The DSM-5 also provides examples of behaviors that may be indicative of ADHD, including frequent fidgeting, excessive talking, difficulty waiting for a turn, an inability to play quietly, and frequent interruption of others [1]. Many remark that these symptoms are merely traits of being a child and are not signs of a disorder. Accusations of ADHD’s overdiagnosis have been on a rise in recent years, as have diagnosed cases of ADHD. In 1997, the parent-reported percent of children with an ADHD diagnosis in a National Health Institute survey was just under 6%. Ten years later, this figure had risen to 10% [2]. Similar results have fueled a growing debate as to whether these diagnoses are the result of a widening definition of the disorder or a true increase in those afflicted. 

Identifying Over Diagnosis

The commonly-held notion that ADHD is loosely and  inaccurately diagnosed stems from an assumption that many diagnoses are falsely positive. For ADHD to be justifiably labeled as overdiagnosed, there must be evidence that the total number of false positive diagnoses significantly outweighs the number of falsely negative diagnoses [3]. Such evidence has not yet been discovered, thereby establishing the ability to recognize the factors at play in a potential false positive ADHD diagnosis as vital in gaining insight to the overdiagnosis assumption. 

Potential Components of Misdiagnosis

The relative age of schoolchildren is a common explanation for ADHD misdiagnosis. Numerous studies have found that children who are relatively younger than their classmates are at an increased risk of ADHD diagnosis. In a study conducted within a school whose school-age cutoff is December 31, results revealed that boys born in December were 30% more likely to be diagnosed and 41% more likely to be treated for ADHD than their January-born peers. Girls born in December were 70% more likely to be diagnosed and 77% more likely to be treated for ADHD than those born in January [4]. These findings suggest that diagnostic measures have failed to account for the relative developmental immaturity of young children, leaving unnecessary room for subjectivity in diagnosis. 

Early diagnosis provides another point of concern in the misdiagnosis of ADHD, given that most ADHD research has been conducted on older, school-age children, rather than younger preschoolers [4]. Research as to the manifestations of ADHD at such a young age has been limited. Current diagnostic measures are geared toward older children and may lead to false positive diagnoses, especially considering the prevalence of inattention, impulsivity, and hyperactivity at that developmental age [5]. 

The argument of diagnostic inaccuracy has been substantiated in a number of studies, such as a 1993 study that evaluated 92 children previously referred to a specialized ADHD clinic. Of the referrals, only 22% received a primary diagnosis of ADHD and only 37% were given a secondary diagnosis [3]. Variability in assessment among providers may be to blame for these diagnostic inaccuracies that may contribute to an increase in false positive diagnoses. 

Potential gender differences in the manifestations of ADHD may be at blame for deflated diagnoses in girls. It has been hypothesized that boys tend to exhibit the prototypical characteristics of ADHD through disruptive and hyperactive behaviors. Girls, however, may exhibit less externalized and disruptive behavior that had become characteristic of ADHD and increased intellectual impairment [4]. A potential inability to distinguish between different manifestations of the disorder suggests further inaccuracy in the diagnostic criteria. 

Conclusion

It appears to be overwhelmingly evident that ADHD is often misdiagnosed. Fallacies in the diagnostic criteria may be to blame for an inflated number of diagnoses in preschool-age children and developmentally immature children, as well as a deflated number of diagnoses in girls. Although such diagnostic concerns have been supported by a number of studies, sufficient evidence for systematic overdiagnosis remains lacking. Due to the variability in assessment techniques by provider, prevalence rates of ADHD are unreliable and cannot be used to prove that the number of false positive diagnoses drastically outweigh the number of false positive diagnoses. Despite this, the popular idea that ADHD is widely misdiagnosed remains intact, and likely will remain as such. It is important to remember that such claims are generally based on unreliable data and should be deemed untrustworthy by association. 

Alaina Buerger, Youth Medical Journal 2022

References

[1] Reynolds, Cecil and Kamphus, Randy. “Attention-Deficit/Hyperactivity Disorder (ADHD).” DSM-5 Diagnostic Criteria, Pearson, 2013, http://images.pear sonclinical.com/images /assets/basc -3/basc3resources/DSM5_DiagnosticCriteria_ADHD.pdf

[2] “Attention-Deficit/Hyperactivity Disorder (ADHD).” Centers for Disease Control and Prevention, 23 September 2021, https://www.cdc.gov/ncbddd/adhd/timeline.html

[3] Scuitto, Mark. “Evaluating the Evidence For and Against the Overdiagnosis of ADHD.” Journal of Attention Disorders, Sage Publications, September 2007, pp. 106-113, https://t heunbrokenwindow.com/wp-content/uploads/2017/10/ADHD-Overdiagnoses.pdf

[4] Ford-Jones, Polly Christine. “Misdiagnosis of attention deficit hyperactivity disorder: ‘Normal behaviour’ and relative maturity.” Paediatrics & child health vol. 20,4 (2015): 200-2. doi:10.1093/pch/20.4.200

[5] Tandon, Mini et al. “Attention-deficit/hyperactivity disorder in preschool children: an investigation of validation based on visual attention performance.” Journal of child and adolescent psychopharmacology vol. 19,2 (2009): 137-46. doi:10.1089/cap.2008.048 

The Brain: How does it actually work?

The brain, arguably it’s the human body’s most unexplored organ. That’s because it’s a very complicated organ that controls every possible aspect of our life. The way we think, how we feel, touch, see, and even something as simple as breathing, letting us stay alive every second. 

The brain is made of about 60% fat and the rest is water, protein, carbohydrates, and salts. Before understanding the way the brain works, understanding the anatomy of the brain is important. The most common misconception of the brain is that it is a muscle. However the brain is an organ made up of nerves. The brain appears to the untrained eye as a pink glob. If you simply look up the structure of a brain, you’ll see a pink glob with portions that are color coded and each of which is accountable for a specific function. That being, there are three main structures that make up the brain, the cerebellum, cerebrum, and brain stem. 

The cerebral cortex is a part of the cerebrum, which is the front of the brain. This section accounts for thinking, emotion, problem-solving, and personality. The folds of the cerebral cortex completely enclose the cerebrum. Additionally, this region of the brain accounts for 50% of the weight of the entire brain due to its huge surface area.

 The cerebral cortex covers the cerebrum and has four lobes. The frontal, temporal, parietal, and occipital lobe. These lobes are in charge of their own activities in the brain. For example the frontal lobe is responsible for language, and other cognitive functions, the temporal lobe (which contains the wernicke area, helping humans understand language) plays a major part in visual perception and hearing, the parietal lobe porches what they see or hear, leaving the occipital lobe to interpret visual information as it also contains the visual cortex. The cerebral cortex’s right hemisphere, also referred to as the right side, governs the left side of the body, while the left side (or left hemisphere) governs the right side. The corpus callosum, a bridge of white matter, connects the two hemispheres (or sides) of the brain. The cerebrum and spinal cord are linked via the brainstem. The brainstem is made up of the midbrain, pons, and medulla. The midbrain aids in awareness and helps you respond to environmental changes, such as potential threats.

The pons have multiple functions, including blinking, facial expressions, and focusing vision. Ten cranial nerves arise from the pons which connect to the face, neck, and trunk. 

The medulla regulated the biological functions which are key for survival such as heartbeat, blood flow, and breathing. This part of the brain detects changes in blood oxygen and CO2 levels. Swallowing, coughing, and vomiting also originate from the medulla. 

Lastly, there’s another section of the brain called the cerebellum, also known as the “little brain”. It’s stuffed underneath the cerebrum at the back of the head. It regulates balance, and movements we’ve learned, like fastening buttons. However, it cannot initiate the movements, it just manages them. The cerebral cortex developed on top of the cerebellum, an ancient portion of the brain, as humans developed. 

There is no single “centerpiece” for the brain. No particular part of the brain acts as a control system that merges signals from various regions. However, instead, multiple connections form a dense network that overlaps between the different regions. Your brain contains billions of nerve cells that are arranged in patterns that coordinate actions and thoughts. Nerves work similar to an electrical circuit, if the brain is considered a big computer. The brain processes information that it receives from the senses and body and sends messages back to the body through the help of nerves. However, in biology, electricity is the movement of charged particles (ions) through a cell’s membrane, also known as the surface layer. An electrical wave travels the entire length of a neuron, also known as a nerve cell, due to the movement of ions. This neuron has longer branches that send messages and shorter branches that receive signals, resembling a tree (called an axon). And at the ends of axons known as synapses, electrical messages leap from one neuron to another. This results in the generation of a fresh electrical wave in that neuron via the release of chemical signals called neurotransmitters. The little chemical neurotransmitters are then released by the neuron in response to the electrical wave at the synapses, where they travel to other cells to connect proteins on their membrane-like cell surfaces. Our muscles receive instructions from our neurons about when to move in this way.

References: 

https://www.hopkinsmedicine.org/health/conditions-and-diseases/anatomy-of-the-brain

https://www.webmd.com/brain/picture-of-the-brain

Functions of the Brain

https://www.aans.org/Patients/Neurosurgical-Conditions-and-Treatments/Anatomy-of-the-Brain

Brain Structure And Function

https://nida.nih.gov/videos/human-brain-major-structures-functions

https://www.mayoclinic.org/brain/sls-20077047?s=3

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7725213/

When is the Next Pandemic after COVID coming? Sorry, it’s already here.

Bill Gates warned us that it was coming. Five years ago, Microsoft’s co-founder and multi-billionaire warned the world about an impending global pandemic during a Ted Talk, which has now amassed over three billion views worldwide. In the talk titled “The next outbreak? We’re not ready.”, Gates discussed the lessons learnt from Western Africa’s 2014 Ebola crisis and declared that international governments were not prepared for the foreseeable pandemic that would hit them.

Sadly, Bill Gates was right. On January the 5th, 2020, the COVID-19 virus was officially declared a global healthcare level threat by the World Health Organisation and now almost two years in, we are not yet clear of this one-in-a-generation global contagion.

So, if Gates was right the first time when should expect the next pandemic?

Unfortunately, it is bad news for us……. The next pandemic is here already and unfortunately, we don’t have any vaccines or monoclonal antibody therapy to fight it. The death rates that come with it will be higher than COVID 19, and social distancing or lockdowns will only make it worse. Because this time the cause is not an infective viral disease, it’s a mental health pandemic.

And just because this pandemic is not caused by an infection, it doesn’t mean that it won’t be more devastating if we don’t deal with it in time.

What are the common mental health impacts of the COVID-19 pandemic?

Due to the COVID 19 pandemic, there has been an exponential increase in the number of mental health problems reported over the past 18 months. An investigation conducted by Statista showed that the percentage of adults living in the United States displaying symptoms of anxiety and/or depressive disorder tripled between 2019 and 2020, increasing from 11% to 42.4%.

So what does mental health got to do with a viral infection? You never hear of it this issue when it’s influenza season.

Quite simply, this COVID 19 pandemic has been longer, harder, and far more damaging than we could ever have imagined. Although whilst people like Bill Gates have said that should have been prepared for such events, even they could not have predicted the severity of this once-in-a-generation pandemic.

Similarly, the mental health effects of COVID 19 are also more profound than usual and can even affect those who don’t actually contract the virus. The devastating problem with mental illness is that, unlike other medical conditions, it does not just affect the one person, but also has a knock-on effect on those around them, especially close family members. In this regard, it is more “infectious” than the virus itself. A WHO report suggests that mental health issues play a part in the death of over 40% of individuals and those with mental health disorders tend to die 5 years earlier than those not afflicted.

From an individual standpoint, COVID can have several ways to exert its effect on mental health. Firstly, just contracting the virus can cause the patient to feel stigmatized especially if they pass it on to family or friends. The sense of harming a loved one especially if it causes the death of that person will have a devastating effect on the person’s psyche.

Secondly, if the patient develops severe symptoms of COVID, especially for those who need intensive care, they will be forced, for maybe the first time, to face their own mortality. The elation of survival can be quickly replaced with the horrors of the near-death experience, similar to those who suffer from post-traumatic stress disorder.

Finally, the COVID 19 virus can have long-lasting medical effects for those who do contract the virus. From research so far, up to 1 in 3 people who have contracted COVID described experiencing lethargy, persisting pains as well lingering neurological and cognitive symptoms such as difficulty thinking and fumbling over simple words. Whilst it appears that most eventually will “shake off” these effects, it is believed that for a small number, this may become a chronic condition. The loss of self-worth associated with this, for the individual, is incalculable.

These effects have been even worse for members of the healthcare profession. Faced with the initial unknown nature of the pandemic and the lack of adequate protective equipment, frontline medical workers have been described as “ being on their knees” in response to the crisis by media representations, with many warning us of an even worse mental health epidemic amongst the frontline healthcare workforces.

For the most part, healthcare workers are psychologically resilient professionals highly trained to deal with death and loss. But the elevated death toll, mental and physical burnout from working overtime, and the constant stress on their own safety and the people around them have undoubtedly placed healthcare workers at additional risk for developing mental health problems. The magnitude of the sacrifices made daily by these dedicated people will not be without consequences. In fact, prior to the pandemic, this group was recognized as having the highest rates of stress, mental burnout, drug and alcohol dependence and high suicide rates. Large numbers of individuals working long-term in the NHS have quit their jobs and the loss of this talent will need time and resources to replace.

From a family standpoint, COVID has created a different, but no less devastating effect on mental health. One of the most direct manifestations of this is due to the infective nature of COVID 19. Many relatives have been unable to comfort, personally care for or be able to be at the last moment of a loved one that unfortunately lost their battle with the virus. Being able to care for and say goodbye to a family member can be a great help in the grieving process. Being robbed of this “sense of closure” is likely to make the grieving process harder and further increase the mental burden on surviving family members.

Lockdown itself has caused a number of interpersonal issues. The rates of domestic violence, separations and divorce filings have skyrocketed over the past 18 months. Families who were able to co-exist happily with each other during a normal routine found themselves unable to tolerate each other when they have to be together 24/7. Physical violence both for the victim and the perpetrator can carry a high mental toll and the ensuing separation and divorce is likely to widen the psychological damage to the entire family unit, especially the children. If unresolved, these children could potentially carry the scar of this trauma into their own adult lives and perpetuate this trauma for the next generation.

With the global lockdown has come the massive global recession which has hit world economies and the financial status of everyone around the world. Many people have lost their jobs and with it their financial stability and self-esteem. It is well known that depression and unemployment go hand in hand and with millions out of a job, this has added further to the mental health burden of those affected.

So how do we deal with this?

The difficulty in tackling this mental health pandemic is the common misconception that most believe “it won’t affect me”. Most sufferers will be in denial that they have a mental health problem. But the first step in dealing with any problem is to first admit that there is one.

So, in order for any solutions put in place to be fully effective, responses from local, nationwide, and worldwide representations must be called on to collectively decide on how best we can educate the public about the current pandemic on our mental health and come up with strategies to tackle the inevitable mental health crisis coming our way. Without public education, those affected just will not recognize that they have a problem.

Given that the majority of psychological cases will be dealt with by emergency first-responders and frontline healthcare workers with relatively low experience in mental health, many cases may be missed at the patient’s first time of contact with the medical profession.

The creation of specific guidelines must be set out by health departments and governments to help all first responders and frontline healthcare workers seamlessly diagnose, care for, and treat patients with psychological illnesses. Increasing direct access to mental health care professionals and informing the public how they can do so will also help to reduce the number of those who “slip through the net”.

Healthcare workers, teachers and governments are well-positioned to support students, patients, and the general public during this trying time. Simple solutions such as offering stress management and coping methods to the public/ students at schools should be put into effect as soon as possible. Increasing the availability of walk-in appointments with a mental health specialist in schools and workplaces will also help decrease the number of undiagnosed mental illnesses and new psychological problems being developed.

Addressing the social stigma associated with such illnesses must be another first step taken by governmental bodies, influencers and people in higher positions when tackling this crisis. People suffering and living with mental health issues should stop feeling ashamed of their condition and speak out about their own experiences to inspire others to see mental health specialists if needed.

As for hospital staff and health departments, there are a number of strategies they can implement, to ensure that patients in their wards are as well-supported as possible. For example, panic-inducing news channels constantly bombarding us with statistics on death tolls and the pandemic should be turned off. The staff can instead encourage patients to engage in mindful activities such as reading, solving puzzles and non-strenuous exercise. It is important that nurses who have direct contact with patients try to understand the world from their patient’s perspectives and tailor their care accordingly.

For better or for worse, the COVID-19 pandemic has changed us, the people around us and the world around us. But as we come closer to reaching herd immunity and a possible end to the COVID 19 pandemic, it is paramount that, more than ever, we do not turn a blind eye to the mental health crisis brewing just beneath the surface.

Dealt with wrongly, the mental health pandemic could be more devastating than the COVID pandemic we are facing now.

——

Works Cited

1.  Business Insider. 2021. Mental health problems to be next pandemic after COVID-19 crisis, says study. [online] Available at: [Accessed 13 November 2021].

2.  Dias, M. and Bunn, S., 2021. Mental health impacts of the COVID-19 pandemic on adults. [online] POST. Available at: [Accessed 13 November 2021].

3.  Mind.org.uk. 2021. [online] Available at: [Accessed 13 November 2021].

4.  Governmentevents.co.uk. 2021. Flattening a Different Curve: A Blueprint for Covid-19 Recovery? – Government Events. [online] Available at: [Accessed 13 November 2021].

5.  Daily Maverick. 2021. Sponsored Content: Is Mental Health the next pandemic?. [online] Available at: [Accessed 13 November 2021]