Biomedical Research Neuroscience

‘Patient H.M’ – An unsung hero: The forgotten man who forgot everything

By Asmita Anand

Published 4:40 PM EST, Sun May 23, 2021


In recent decades, scientists have made huge progress discovering how our identities, and memories are made and stored. A patient that transformed our understanding of the way  memory functions are organised in the human brain, is  referred to as ‘the man who couldn’t make memories’; Henry Molaison possessed one of the most famous brains worldwide and bestowed unique insights into the inner-workings of human brains.

Who Was He?

Figure 1: HM in 1953 before his surgery (

Henry Gustav Molaison, also known in medical literature as patient H.M. to protect his identity, was born on February 26, 1926 in Manchester, Connecticut.

As a child, he had a relatively normal childhood. Although it wasn’t long after a minor head injury and a family history of seizures (although the exact aetiology behind his seizures remains uncertain), that Molaison began suffering from severe epilepsy. At the age of 10, he started having absence seizures and 6 years later he developed generalised tonic-clonic seizures. His seizures greatly impacted his daily life and led him to drop out of high school. Later he was also unable to maintain his job and function independently. Molaison’s case was so severe that it couldn’t be treated pharmacologically with high doses of anticonvulsant medication.

After nearly 10 years he turned to Dr William Scoville, a renowned daredevil neurosurgeon of his time, with hope to lead a normal life once again. At the age of 27, his hippocampus was removed in an experimental procedure in an attempt to alleviate the impact his seizure had on the quality of his life. He underwent a ‘bilateral medial temporal lobectomy’, which surgically removed the medial temporal lobe on both sides of his brain. This included the hippocampal complex, parahippocampal gyrus, the uncus, the anterior temporal cortex, and the amygdala, according to Scoville’s own illustrations of his surgical technique. However in around 1992-199, MRI scans revealed that the surgery was less extensive than he thought, but enough to cause the damage it did. [1]

Figure 2: Diagram depicting HM’s brain after surgery compared to a normal human brain (

Although Dr Scoville hoped it would cure the epilepsy, he still wasn’t completely sure whether it would be successful or if there might be any long lasting side effects of this procedure. As a result, both of his thoughts were correct. Molaison’s seizures had stopped but unfortunately he was also left with long term memory loss, leaving him constantly living in the present tense. Later Scoville admitted that the operation was a tragic mistake and has spoken strenuously about the dangerous implications of bilateral mesial temporal lobe surgery.

Different types of Amnesia

There are multiple types of amnesia, such as Retrograde, Anterograde, Transient global and Infantile amnesia. Retrograde amnesia is when someone is unable to recall events that occurred before the development of the amnesia and is commonly used in films and media. [2] Whereas anterograde amnesia refers to a decreased ability to retain new information and is typically caused by brain trauma. [3]

Molaison developed a peculiar form of amnesia and suffered from both partial retrograde amnesia and anterograde amnesia. The latter meant he lost the ability to form new memories, such as the inability to remember what he had eaten for lunch that day, tests that he just done minutes before and names he had just been introduced to. Scoville wrote: “After operation this young man could no longer recognise the hospital staff nor find his way to the bathroom, and he seemed to recall nothing of the day to day events of his hospital life. There was also a partial retrograde amnesia.” [4] This meant that while he could recall memories from his childhood, he was unable to remember almost 11 years of events prior to the operation. 

However, both his personality, intellectual abilities and perception remained unaffected and his IQ increased from 104 to 117. [5] Molaison still had the ability to form non-declarative memories, allowing him to still acquire and develop motor skills, which led to Brenda Milner’s discovery of the distinction between procedural and declarative memories. While his mind became like a sieve, through other testing performed by Milner she discovered that he still possessed short term memory. This led to the notion that this too existed in a separate brain structure to the one he lacked.

Short Term and Long Term Memory

Molaison’s misfortune ended up as a milestone in our understanding of the brain as up until it occurred memory wasn’t thought to be localised in one area of the brain. Dr Scoville and Brenda Milner were the first to make observations and report his case in 1957 in the “Loss of recent memory after bilateral hippocampal lesions”. Since he had difficulty remembering doing the tests in the day, Molaison never grew tired of the numerous experiments he partook in.

It is thanks to Molaison, that today we know that intricate functions are directly connected to distinct regions of the brain. The hippocampus, which is embedded deep into the temporal lobe, plays an important role in forming, retaining, and recalling declarative memories and spatial relationships. It’s also where short-term memories are turned into long-term memories.

Five decades later, referred to as Patient H.M., Molaison’s case grew in popularity due to the publication, which has thoroughly been cited numerous times. Researchers arrived at the conclusion that short term memory was not connected in any way to the medial temporal lobe structures. A particular researcher out of the 100 who studied him, Suzanne Corkin, spent the most time with Molaison interviewing him and working with him for 46 years. In her book “Permanent Present Tense: The man with no memory, and what he taught the world”, Dr Corkin covers how Molaison’s mind was used to understand how our minds and memory work. It also covers his early life and key childhood memories from their personal conversations or careful reporting and research. She wrote about how she went from viewing him as a “subject” to seeing him as a human being. Molaison’s life was not easy as he often struggled at times. After a while he came to understand that while others could retrieve and store memories, he could not. Nevertheless, he remained positive, coping well with his difficult situation and he acts as a true inspiration for his extreme resilience. H.M. once poignantly remarked that “every day is alone in itself. Whatever enjoyment I’ve had, and whatever sorrow I’ve had”. [6] 

His Legacy

Figure 3: Photography by Spencer Lowell (

Sadly Henry Molaison passed away at the age of 82 due to respiratory failure. Despite his death in 2008, his brain still continues to excite and offer further investigation into memory as there is still much to uncover. Mr Molaison was much, much more than a research specimen but a person who despite facing grave misfortune, still managed to show ‘the world you could be saddled with a tremendous handicap and still make an enormous contribution to life.’ [7] Columbia pictures and Scott Rudin have even acquired rights to develop a film based on his life.

As Dr Corkin described as “a beautiful finale to his enduring contributions”, his frozen brain was cut into 2,401 slices postmortem, which have been photographed and digitised into a high-resolution, 3D model for further anatomical analysis, in which we can even view individual neurons!

Molaison once commented: “It’s a funny thing – you just live and learn. I’m living and you’re learning.” Henry Molaison leaves behind a legacy (quite literally through the preservation of his brain!) which shall be remembered by us all and stay within our own memories. His forgetfulness has revolutionized our understanding of the brain, which we can still learn so much from till this date.

To end, as Dr Corkin said “Henry’s disability, a tremendous cost to him and his family, became science’s gain”.

Asmita Anand, Youth Medical Journal 2021 


[1] Annese, J. (2014, January 28). Postmortem examination of patient H.M.’s brain based on histological sectioning and digital 3D reconstruction. Nature Communications.

[2] I. (2020, November 25). Retrograde Amnesia | Symptoms, Causes, Illness & Condition. The Human Memory. amnesia is a form,that occur after the onset

[3] Cherney, K. (2018, September 18). Anterograde Amnesia. Healthline. amnesia refers to a,is a subset of amnesia.

[4] Lichterman, B. (2009, March 17). Henry Molaison. The BMJ.

[5] Scoville, W. B., & Milner, B. (1957, February). Loss of recent memory after bilateral hippocampal lesions. NCBI.

[6] Loring, D. W., & Hermann, B. (2017, June). Remembering H.M.: Review of “PATIENT H.M.: A Story of Memory, Madness, and Family Secrets”. Archives of Clinical Neuropsychology.

[7] Adams, T. (2018, March 22). Henry Molaison: the amnesiac we’ll never forget. The Guardian.

Halber, D. (n.d.). The Curious Case of Patient H.M. Brainfacts.

Gholipour, B. (2014, January 28). Famous Amnesia Patient’s Brain Cut into 2,401 Slices. Livescience.Com.

Shah, B. (2014b, July 1). The study of patient henry Molaison and what it taught us over past 50 years: Contributions to neuroscience Shah B, Pattanayak RD, Sagar R – J Mental Health Hum Behav. Journal of Mental Health and Human Behaviour.;year=2014;volume=19;issue=2;spage=91;epage=93;aulast=Shah

Hodges, J. R. (2013, November 23). Memories are made of this. Oxford Academic.

Shapin, S. (2017, June 19). The Man Who Forgot Everything. The New Yorker.

Billington, A. (n.d.). Scott Rudin Developing Feature Film About Henry Molaison. FirstShowing.Net. a cue from The,in medical circles as H.M.


Subliminal Stimuli and its Neurological Affects

By Neha Menon

Published 6:12 PM EST, Fri April 16, 2021


Subliminal messages have been used since time immemorial, but researchers are yet to give a very concise explanation of, both, whether it works and if it does, how? In simple words, “any sensory stimuli below an individual’s threshold for conscious perception is called a subliminal message.” (Wikipedia)

Consciousness, put very plainly, is the state of being aware – aware of one’s surroundings, thoughts, emotions and the external & internal environment. On the contrary, the unconscious state of mind is one wherein there lies “a reservoir of feelings, thoughts, urges, and memories that are outside of one’s conscious awareness.”[1] This consciousness is enabled by the part of our brain called the cerebrum, whereas the unconscious actions are performed by the basal ganglia and cerebellum. This concept may be  attributed to Sigmund Freud – Austrian neurologist and the founder of psychoanalysis. The discussion of the conscious and unconscious state of our mind highlights the core topic of this article: subliminal primings or subliminal messages, which were brought to the mainstream media as early as 1957.[2]   However, extensive research and scientific opinions on this subject have only emerged in the recent years. This is discussed in further topics.

Primarily, subliminal messages work by nudging your unconscious. This would imply that by listening or looking at a subliminal message, we are gathering information or getting affected unconsciously. This is why, before we look at the ‘what, why and how’ of subliminal priming, we must understand the theories of the unconscious state of mind, which will give a great deal of insight regarding the direct workings of a subliminal message on the brain.

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“The mind is like an iceberg, it floats with one-seventh of its bulk above water.” — Sigmund Freud.

The Unconscious State of Mind

It would be beneficial to understand first that the conscious state of mind is finite. If we were to notice and process (consciously) everything that we see, hear or feel in a day, our brain would be far too overwhelmed and the retention of this information may be compromised. The unconscious, on the other hand, is vast – limitless – to say the least. Everything we see, hear or feel goes into our unconscious but doesn’t necessarily get processed. This means that the way we perceive something may not be the actual reality of it.

Secondly, it is important to note that the brain can only perceive something in the way and form that it first enters our mind. Meaning, imagine a picture, for instance, that could be perceived in two different ways based on how you look at it. Perhaps (as shown in the image below) : an old woman who, if and when the perspective is changed – looks like a young girl. Your brain may be able to identify these two ‘forms’ of the same picture but it will not be able to see both forms at the same time.

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Image credits: public domain

The “How” Of Subliminal Messages

Once we know how the unconscious mind works, we can move on to explore why and how subliminal messages affect our brain neurologically.

In subliminal messages, there are multiple items (audio/video/picture) that require relational processing. This may  be compared to the picture discussed above, which can be seen as two separate images. Relational binding hence calls upon the hippocampus – a complex brain structure embedded deep into the temporal lobe. It has a major role in learning and memory. Hence in this case, it can rapidly store novel relations for a longer term. Usually, it is known that the hippocampus is involved in the encoding and retrieval of consciously perceived information.

“However, growing evidence suggests that hippocampus operates independently of consciousness and that nonconscious relational learning is humanly feasible”[6]

While talking about the direct effects of subliminal stimuli on the brain, they robustly activate certain parts:

Amygdala – It is recognised for its role to process emotions. It is the part of the human brain best known for its ability to drive the ‘fight-or-flight’ response and also plays a vital role in memory. 

Insula – The insular cortex links sensory experience and emotional stimuli. It is also linked with conscious emotional feelings

Hippocampus – It plays a part in memory consolidation: the process of transferring new learning into long-term memory

Anterior cingulate – has been implicated in several complex cognitive functions, such as empathy, impulse control, emotion, and decision-making.

We see that most of the affected parts have a role to play in emotional valence or memory. It is these parts that are activated when your brain is exposed to subliminal messages.

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Subliminal Messages In The 1900’s

When the history of subliminal messages is regarded, we see that most of them were used in marketing, or advertisements. The following timeline shows some of the important milestones in the history of use and discovery of subliminal messages:

1943 – Subliminal messages were occasionally used on the radio and television programs. [3]   

1990 – Many researches showed little or no link in the subliminal messages and the psychology of the brain, while others started uncovering subtle effects. [3]   

2006 – Studies showed and proved that subliminal messages did work in several advertising scenarios.  [3]   

2007 – Subliminal messages for academic performance were uncovered and studied. [3]  

2010-2015 – Imaging proved that subliminal messages did affect several parts of our brain, including but not limited to the visual cortex and hippocampus[3].   

Other common forms of subliminal messages in recent years are:

  • Images being inserted into the frames of movies, trailers, commercials etc., for an extremely short amount of time in such a way that the brain cannot consciously comprehend it.
  • Audio messages inserted under louder audio messages in order to mask it.

The “Why” Of Subliminal Messages

Subliminal messages and stimuli have been used in several places for several different reasons. 

  • The most common of all, is advertising and marketing. Companies like Coca-Cola show a good example of subliminal messaging for marketing in the late 1900s. Here the words “Buy Coca-Cola” and/or “Buy Popcorn” were flashed into movie reels.
  • For political agendas, like the one in the George Bush campaign in 2000. The opponent, Al Gore, accused Republican campaign managers of including a subliminal message in an attack ad focusing on Gore’s proposed healthcare policies. The word ‘RATS’ was flashed quickly right before the presentation of the word ‘bureaucrats’. 
  • In Disney movies like Aladdin, The Little Mermaid and The Lion King. It is unclear what the agenda for these were, and whether they were intentional at all.
  • In more recent times, subliminal messages have been famously used as auditory sources – melodic rhythms in particular. These claim to be able to change several things in your physical and mental realms; from removing mental head-block to changing eye color or weight. It’s efficiency or lack thereof, is not proved yet.


Exposure to subliminal stimuli have been proved to have certain effects on the human brain through research and experimentation. The efficiency, however, is not ensured. According to a UCL research, subliminal messaging is most effective when the message conveyed is negative in comparison to when it is positive. [7] Certain subliminal stimuli (especially now that the concept has taken pace) may have harmful impacts on the brain. They cannot damage the brain per-se, but can have negative impacts on your subconscious mind.

Neha Menon, Youth Medical Journal 2021


Cherry, K. (2020, December 09). The Structure and Levels of the Mind According to Freud. Retrieved from[1]

6 Examples of Subliminal Advertising, from Spooky to NSFW. (n.d.). Retrieved from [2]

Stern, V. (2015, September 01). A Short History of the Rise, Fall and Rise of Subliminal Messaging. Retrieved from [3]    

Sigmund Freud. (n.d.). Retrieved from [4]  

Subliminal stimuli. (2021, February 16). Retrieved from [5]

Ruch, S., Züst, M. A., & Henke, K. (2016, August 20). Subliminal messages exert long-term effects on decision-making. Retrieved from[6]Ucl. (2018, November 15). UCL study: Subliminal messaging ‘more effective when negative’. Retrieved from [7]


Your Brain Is Built To Forget

By Neha Menon

Published 4:38 PM EST, Sun March 28, 2021


The theory of memory, its stages, and mechanisms have been an ever-changing topic of discussion and research throughout the years. However, it has always been known that there exist certain loopholes and gray-areas which causes a related phenomena: forgetting. Through the years of study in cognitive psychology & neurology, the process of forgetting was always treated as an afterthought. In contrast to this, more recent studies contradict decades-old assumptions. Specifically they prove that the brain was, in fact, built to forget. That, in order to remember, forgetting is a crucial step.


Much is still to be learned about memories; how they are created, accessed and, sometimes, lost. But the little that we do know is important to note before studying the significant phenomenon of forgetting. 

  • When we talk about the process of memory, it is imperative to understand that what we hear, see or learn does not simply go into the brain unedited as a recording. It is, in fact, constructed and reconstructed several times by what we hear or learn after that. 
  • Although we may think that the memory of some people is near-perfect, our active cognitive processing of information ensures that memory is never an exact replica of what we first picked up, learned, or experienced.
  • The physical basis of memory is that these higher intellectual processes are based in the cerebral cortex. “If certain parts of the cerebral cortex are stimulated electrically, there will be recall of experiences.”[1]  It is commonly known that the process of memory entails encoding, retaining, and retrieving information. Other parts that are actively involved in these activities are the amygdala, the hippocampus, the cerebellum, and the prefrontal cortex.
  • Autobiographical memories (personally experienced events) develop in the hippocampus, while the actual encoding of memory takes place through synaptic plasticity wherein “neurons constantly produce new proteins to remodel parts of the synapse, which enables the neurons to selectively strengthen their connections with one another”[2]
  • The crux of the topic is this: “Memory is the means by which we draw on our past experiences in order to use this information in the present.” (Sternberg, 1999).
Memory & The Brain | Where Is It Stored & How Is It Used?
Parts of the brain involved with memory

Forgetting: A function of memory, not a failure of it.

The mechanisms of forgetting have been researched and studied in flies and rodents. One major takeaway from what was learned is the effect of AMPA receptors. AMPA receptors are particular types of receptors found at the synapse of a neuron, and the amount of this receptor in a synapse determines connection strength between neurons. Essentially, the strength between neurons is directly proportional to the effectiveness of the encoding process of some memory.

If the synapse of two neurons has the necessary amount of AMPA receptors, it is a given that the strength between these two neurons is good, and in effect, the memory has been encoded properly. The problem is that none of these AMPA receptors are stable. “They are moved in and out of the synapse constantly and turn over in hours or days.”[2]

Hardt, a researcher, proposed that AMPA receptors can also be removed, which would mean that forgetting is an active process. And if that were true, then preventing the removal of AMPA receptors should prevent forgetting. When this was tried on rats, it seemed as though for the rat to forget, it had to continually destroy certain connections at the synapse. With this, Hardt says, “Forgetting is not a failure of memory, but a function of it”.[2]

Another proposed cause of forgetting was seen by Paul Frankland, a neuroscientist. He discovered that increasing the neurogenesis in mice caused them to forget more. This is, in fact, very ironic and contradictory to what we know about neurogenesis: it is the process by which new neurons are formed. New neurons should ideally mean more capacity to store memory. But the effect of neurogenesis on its proportional loss of memory was explained: “When neurons integrate into the adult hippocampus, they integrate into an existing, established circuitry. If you have information stored in that circuit and start rewiring it, then it’s going to make that information harder to access,” Frankland said.

Humans keep the memories accurate by forgetting | Lunatic Laboratories


There are certain other known theories regarding the process of forgetting: dopamine receptors and M.C.H neurons are a few amongst some others. 

Researchers like Ronald Davis believe that the brain employs forgetting and therefore clear out unnecessary pieces of information in order to make retaining other ones easier. This would imply that the brain keeps memories accurate by forgetting other less-important ones. Others also see forgetting as an advantage for the mental flexibility inherent in creative thinking and imagination.[3]

Neha Menon, Youth Medical Journal 2021


Chawla, D. S., & Quanta Magazine moderates comments to facilitate an informed, S. (n.d.). To Remember, the Brain Must Actively Forget. Retrieved from

Contributors, H. (2009, October 05). Memory. Retrieved from [1]

Gravitz, L. (2019, July 24). The forgotten part of memory. Retrieved from [2]
Sheikh, K. (2019, September 19). Scientists Identify Neurons That Help the Brain Forget. Retrieved from[3]


Your Brain On LSD

By Neha Menon

Published 4:30 PM EST, Fri February 26, 2021


LSD (Lysergic acid diethylamide) is one element of a wide ranging group of drugs called psychedelics. The primary use of psychedelics is to trigger “non-ordinary states of consciousness”[6], and to alter several cognitive functions such as perception and mood (Wikipedia). LSD specifically works by triggering hallucinations, hence being known as a hallucinogenic drug. But what exactly does LSD do to the human brain? And how can it potentially be used to ease the struggles of thousands of depressed individuals? 

LSD – A Brief History 

In 1938, Swiss chemist Albert Hoffman synthesized LSD for the first time. The fungus that LSD was taken from is said to cause convulsions, madness, and even death. Fun fact: April 19th is still celebrated as “Bicycle Day” in honor of the famous day on which Hoffman rode his bike home after taking LSD for the first time, and experienced an insane inward “trip.” In 1947, Sandoz Laboratories encouraged the intake of LSD by advertising it to be “a cure for everything from schizophrenia to criminal behavior, ‘sexual perversions’ and alcoholism”[6]  (Wikipedia).

It was soon discovered that as little as 25 micrograms of LSD is enough to stimulate vivid hallucinations. The official ban of this drug in the United States in 1967 shows how widely it was abused–while some used it to escape reality, others (specifically the military) began exploring its potential as a chemical weapon. However, many had begun noticing that the use of LSD caused them severe anxiety and depression, while others reported being unable to feel “normal,” and feeling a sense of disconnection from reality.

How LSD Produces Hallucinations 

Firstly, it is important to understand that LSD works by affecting several nerve receptors, such as the dopamine, adrenergic, and serotonin receptors. The last one is particularly interesting and relevant to the functioning of this drug. There is a type of serotonin, known as 5-HT2A, that has a role in the visual cortex. When inside you, LSD affects this particular cell surface receptor. This is the primary cause for the “trippy” visuals.

LSD study reveals why acid trips last so long | Drugs | The Guardian
Photograph: Fredrik Skold/Alamy

The Inner-Workings of LSD 

How exactly LSD affects the brain, and why it gives the results it does, have been subjects of study throughout the years. Researchers from Imperial College London, along with Beckley Foundation, have successfully visualized these effects, and the findings were published in Proceedings of the National Academy of Sciences (PNAS). The following are some major takeaways:

  • Although visuals images are typically processed in the visual cortex, several other brain areas contribute to processing visuals when your brain is on LSD. 
  • In Dr. Robin Carhart-Harris’ words: “We observed brain changes under LSD that suggested our volunteers were ‘seeing with their eyes shut’; as in, they were seeing things from their imagination rather than from the outside world.” [2] 
  • The research group also observed that, despite the volunteers’ eyes being closed, the part of the brain involved in visual processing was accompanied by many other parts of the brain. Furthermore, the size of this effect correlated with volunteers’ ratings of complex, dreamlike visions, meaning that complexity was directly proportional to the involvement of other parts of the brain. 
  • Visuals are processed in the visual cortex, movement in the cerebellum, and hearing in the auditory cortex. Notice that these are individual and separate areas of the brain. While on LSD, the level of ‘separateness’ is lower, and the processing of several functions may overlap one another, or unify. 
what does it feel like on an acid trip?

How LSD May Potentially Treat Mental Illnesses

After learning how LSD drastically alters one’s state of consciousness, how is it that this potent psychedelic can be used in treating depression? A lot more research is required to fully understand this (since, as seen in the above image, depression is a potential side effect of the extreme use of LSD), but one of the known  methods is: micro-dosing. People such as Ayelet Waldman–an author who had personal experience with the subtle effects of LSD under smaller doses–believe micro-dosing can help a depressed individual feel better while avoiding hallucinations as a side effect. It may also provide enough of a sense of disconnection from reality to make one’s intrusive thoughts less overwhelming. It is important to note that LSD depression therapy is only available to those who sign up for clinical trials.

Dangers & Disadvantages of LSD Treatment

The effects of LSD–both negative and positive–have yet to be researched thoroughly enough. In my opinion, the use of the drug to cure depression is very risky. Different drugs produce different levels of compatibility amongst a large, diverse population. And, in this case, the difference between a ‘good’ versus a ‘bad’ trip may be too big of a risk for someone with an already compromised state of mental health to undertake. Serious side effects such as increased anxiety, or potentially violent depressive episodes due to flashbacks from bad experience with the drug are to be wary of.

Note: LSD is known to have several side effects on the brain, both short term and long term. It is illegal to sell or intake LSD in most places, so self-treatment or ingestion is not recommended. 

Neha Menon, Youth Medical Journal 2021


Foundation for a Drug-Free World International. “The History of LSD – Acid, Albert Hoffman & Timothy Leary – Drug-Free World.” Foundation for a Drug-Free World, Accessed 21 Feb. 2021. [1]

Neuroscience News. “This Is Your Brain on LSD.” Neuroscience News, 12 Apr. 2016, [2]

Sample, Ian. “Why Does LSD Make You Hallucinate?” The Guardian, 22 Feb. 2017, [3]

The Recovery Village. “LSD and Depression.” The Recovery Village Drug and Alcohol Rehab, 15 Jan. 2020, [4]

Wendorf, Marcia. “The Resurgence of Psychedelics: Magic Mushrooms and LSD.” The Resurgence of Psychedelics: Magic Mushrooms and LSD, 9 Aug. 2019, [5]Wikipedia contributors. “Psychedelic Drug.” Wikipedia, 17 Feb. 2021, [6]


Neuroinfectious Diseases


Neuroinfectious diseases result when the body’s immune system is weak to fight off pathogens or germs. These diseases are caused by bacteria, viruses, fungi, etc. There are many of these infections that can affect the nervous system. Some of the most common symptoms are pain, swelling, redness, impaired functions, etc. These infections can be usually treated by doctors who are trained in infectious diseases. Some of the common neuroinfectious diseases are Encephalitis, Meningitis, and Transverse myelitis.


Encephalitis is an infection of the brain, which can either be caused by bacteria or virus. The most common cause of encephalitis is by a viral infection. Some of the viruses that cause encephalitis are enteroviruses, tick-borne viruses, herpes simplex virus, etc. The 2 kinds of encephalitis are primary encephalitis and secondary encephalitis. Primary encephalitis is when the virus infects the brain. Secondary encephalitis results from damaged immune system reaction somewhere else in the body, and this causes the immune system to attack healthy cells in the brain. The common symptoms of encephalitis are headache, fever, aches in muscles or joints, and fatigue or weakness. Some more severe symptoms of encephalitis are hallucinations, loss of sensation, seizures, loss of consciousness, and problems with speech or hearing. Factors that might increase the risk of encephalitis include age, weakened immune system, geographical regions, and season of the year. There are some ways you could prevent viral encephalitis. Practicing good hygiene such as washing hands with soap regularly and not sharing food utensils are some ways to prevent encephalitis.  


Meningitis is an infection where the membranes that cover the brain and spinal cord become inflamed. Meningitis is commonly caused by viral infection but some other causes include bacterial, parasitic, and fungal infections. The common symptoms of meningitis are stiff neck, sensitivity to light, no appetite or thirst, skin rash, and sudden high fever. Treating meningitis depends on what type of meningitis.  Antibiotics that are directly injected to the vein are used to treat bacterial meningitis. Sometimes doctors will suggest a broad-spectrum antibiotic until they know the exact cause of meningitis.

Transverse Myelitis

Transverse myelitis is when both sides of one section of the spinal cord become inflamed. This neuroinfectious disease cuts off the messages the spinal cord sends throughout the body. Some of the causes of transverse myelitis are infections, immune system disorders, and myelin disorders. Some of the common symptoms of transverse myelitis are pain in lower back, abnormal sensations, and weakness in arms or legs. 

Nitin Beeram, Youth Medical Journal 2021


Encephalitis—Symptoms and causes. (n.d.). Mayo Clinic. Retrieved December 28, 2020, from

Meningitis—Symptoms and causes. (n.d.). Mayo Clinic. Retrieved December 28, 2020, from

 Neuroinfectious diseases. (n.d.). American Brain Foundation. Retrieved December 28, 2020, from

Neurological infections. (n.d.). Retrieved December 28, 2020, from

Transverse myelitis—Symptoms and causes. (n.d.). Mayo Clinic. Retrieved December 28, 2020, from


An Overview of Memory and Amnesia


Often described as simply the partial or total loss of memory, amnesia is one of those conditions we’ve all heard of, have seen in media and can somewhat grasp a hold of what it is.  But aside from just waking up with no recall in movie scenes, in reality, amnesia works in a much deeper and complex manner.

What is Amnesia?

There are two main classifications of amnesia: retrograde amnesia and anterograde amnesia. Retrograde amnesia is when the patient cannot process information and memories typically before the date of what has triggered the amnesia such as an accident or operation. Anterograde amnesia is when new information cannot be transferred from the short term memory store into the long term memory store.  In order to understand how amnesia is affected and affects the brain, you first need to understand how the brain should store memories.

How are Memories Stored in the Brain?

The way memories are processed is not clearly known however there have been several models made by psychologists and neuroscientists.  One of the most commonly referred to encompass the whole is the multi store model (MSM).  This model was curated by Richard Atkinson and Richard Shiffrin (1968, 1971) shows how information flows through the system through processing.

 A stimulus from the environment firstly will pass into what’s known as the sensory register.  Our sensory register has temporary stores for each of our five senses that has a high capacity of approximately one hundred million cells in each eye storing data and information, but it only lasts a period of half a second.  A couple of our biggest is our echoic store, which encompasses auditory information coded acoustically, and an iconic store, which encompasses visual information coded visually.  As our daily lives are full of billions of stimuli, the brain can only usually focus on a couple in order to process on to the short term memory store, hence the key to moving the information on is paying attention to particular stimuli.

Short term memory is a limited capacity store.  Many researchers have studied how large exactly the STM is.  One famous value being Miller’s magic number, 7±2; on average being able to store 5-9 pieces of information.  Information stored in the STM is coded acoustically, meaning that we remember it primarily by how we heard it or how it sounded.  In order for the information to eventually go to the long term memory (LTM) store, it needs to be maintenance rehearsed, otherwise it would last only about half a minute in our STM.

Long term memory store, also known as our permastore is for information that has been rehearsed constantly to the point the information can be remembered and recalled for many years and possibly decades.  The capacity for LTM is proposed to be unlimited.  According to the MSM, memories are ‘retrieved’ from the LTM back into the STM in order to recall it; none of the information is directly from the LTM.

This multi-store model is evaluated as somewhat insufficient as cases of patients with amnesia have proven there to be more stores within the STM and LTM than Atkinson and Shiffrin had proposed.

How Memories are Affected by Amnesia

Curated by Tulving (1985) in response to the MSM not elaborating further on the LTM, are a few different types of memory within long term memory.  They can be classified as declarative, broken down into episodic and semantic memories which you have to consciously think about to recall, and non-declarative as procedural memory, by which you can recall without conscious recognition. 

Episodic refers to our ability to recall from events that occur in ‘episodes’, or events in our daily lives.  These memories are associated to us by time stamps for example recalling something that happened to us last weekend, as well as certain people, places, and behaviours can also be associated to that episodic memory.

Semantic memories are our knowledge of the world, including facts and general knowledge.  These memories are clearly not as personal as episodic as they’re not time stamped, but rather just stockpile if rehearsed enough in your brain.

Procedural memory is also known as muscle memory.  It is our memory of how we physically do things like riding a bike.  Even if we do not ride a bike for an extended period of time, if we learned how to ride it as a child,  it should almost be instant picking it back up later on.  Procedural memories can proceed independently of the brain regions required for declarative memory.  According to fMRI studies, procedural memories activates the basal ganglia, the premotor cortex and the supplementary motor areas in the brain; regions that aren’t typically associated with the processing of declarative memories.

Famous cases of Henry Molaison (H.M.) and Clive Wearing prove that there’s multiple stores of LTM.  Both men were patients with amnesia; Clive had a viral infection in his brain, severely damaging the hippocampus, and Henry had a surgery to cure his epilepsy both resulting in amnesia that affected episodic memories.  They could not recall things they did or what happened to them shortly before, but their semantic and procedural memories were very much intact; Clive could play the piano pieces he knew by heart perfectly and they both knew how to tie shoelaces.  These two cases of amnesiacs had proven evidence the presence of different stores of LTM and they were in different regions of the brain, so if one was affected, the others aren’t  necessarily affected either.


Whilst amnesia detrimentally affects individuals and their loved ones roughly, having patches of memories disappear unbeknownst to the individual, amnesiacs have been one of the biggest contributions to neuroscience, psychology, and the general understanding of memory and how amnesia is initiated in individuals.

Nara Ito, Youth Medical Journal 2021


Atkinson, R. C., & Shiffrin, R. M. (1968). Human memory: A proposed system and its control processes. Psychology of learning and motivation, 2(4), 89-195.

Eichenbaum, H. (1993). Memory, amnesia, and the hippocampal system. MIT press.

Schacter, D. L. (1987). Memory, amnesia, and frontal lobe dysfunction. Psychobiology, 15(1), 21-36.

Aggleton, J. P., & Brown, M. W. (1999). Episodic memory, amnesia and the hippocampal-anterior thalamic axis. Behavioral and brain sciences, 22(3), 425-444.

Hoerl, C. (1999). Memory, amnesia and the past. Mind & Language, 14(2), 227-251.

Nadel, L., & Moscovitch, M. (1997). Memory consolidation, retrograde amnesia and the hippocampal complex. Current opinion in neurobiology, 7(2), 217-227.

Squire, L. R., & Zola, S. M. (1998). Episodic memory, semantic memory, and amnesia. Hippocampus, 8(3), 205-211.

Ryan, J. D., Althoff, R. R., Whitlow, S., & Cohen, N. J. (2000). Amnesia is a deficit in relational memory. Psychological science, 11(6), 454-461.

De Renzi, E., Liotti, M., & Nichelli, P. (1987). Semantic amnesia with preservation of autobiographic memory. A case report. Cortex, 23(4), 575-597.

Lewis, D. J., Misanin, J. R., & Miller, R. R. (1968). Recovery of memory following amnesia. Nature, 220(5168), 704-705.

Snodgrass, J. G., & Corwin, J. (1988). Pragmatics of measuring recognition memory: applications to dementia and amnesia. Journal of experimental psychology: General, 117(1), 34.

Tulving, E. (1985). How many memory systems are there?. American psychologist, 40(4), 385.

Shimamura, A. P. (1986). Priming effects in amnesia: Evidence for a dissociable memory function. The Quarterly Journal of Experimental Psychology Section A, 38(4), 619-644.

American Association for Research into Nervous and Mental Diseases, Squire, L. R., & Zola, S. M. (1997). Amnesia, memory and brain systems. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 352(1362), 1663-1673.

Gazzaniga, M., Ivry, R., & Mangun, G. (2009) Cognitive Neuroscience: The biology of the mind. New York: W.W. Norton & Company.

Squire, L. R., & Alvarez, P. (1995). Retrograde amnesia and memory consolidation: a neurobiological perspective. Current opinion in neurobiology, 5(2), 169-177.

Squire, L. R., & Knowlton, B. J. (1995). Memory, hippocampus, and brain systems.

Scoville, W. B. (1968). Amnesia after bilateral medial temporal-lobe excision: Introduction to case HM. Neuropsychologia.

Wilson, B. A., & Wearing, D. (1995). Prisoner of consciousness: A state of just awakening following herpes simplex encephalitis.


The Link Between Schizophrenia and Neuroplasticity


Schizophrenia is a brain disorder that progresses rapidly after onset with symptoms such as hallucinations and paranoia. It is found in around 1% of the U.S. population – roughly 3 million people. The suicide rate in schizophrenic populations is also alarmingly high, 4.9% higher than the rate of the general population. Literature suggests through improved neuroplasticity, patients suffering from schizophrenia may experience reduced symptoms. Neuroplasticity is the brain’s ability to reorganize itself and reorder its synaptic connections. Examples of neuroplasticity include changes in grey matter, synapse strengthening, and transferring functions to different parts of the brain. The connection between schizophrenia and neuroplasticity has been found that a loss of neuroplasticity results in an increase of schizophrenia symptoms. ​​This claim has been supported experimentally by testing cognitive abilities of schizophrenics vs. non schizophrenics and comparing levels of neural plasticity between schizophrenic and non-schizophrenic patients. Recent studies have shown that drug abuse can negatively impact neuroplasticity, providing a possible relationship between drug abuse and schizophrenia onset in some patients (O’Brien 2009). Use of depressive and excitatory drugs can cause significant effects on pathway formation in the brain, caused by breakdown or creation of new neural synapses. Here we review the role of drug abuse induced changes in neuroplasticity associated with previously reported increases in schizophrenia development.

What is Schizophrenia?

Schizophrenia is a brain disorder that affects around 1% of the United States population with symptoms such as hallucinations, delusions, disorganized behavior, and paranoia. There are many genetic, environmental, and drug use factors that have been shown to contribute to schizophrenia onset. Other possible underlying causes of schizophrenia include pregnancy and birth defects that could be caused by stress inducing factors and epigenetic factors that could arise from environmental factors. Schizophrenia is a progressive disease and tends to deteriorate a patient’s health over time. It is usually diagnosed between the ages of 16-30 and affects both genders but presents in males more often at a ratio of 1:1.4. It is one of the biggest causes of disability worldwide (NIMH 2013). Schizophrenia presents with both positive and negative symptoms; positive symptoms include hallucinations, delusions, and disorganized speech, while negative symptoms include flattened affect, reduced speech, and lack of initiative. It has been found that about 80% of those who stop taking their medications after an acute episode will have a relapse within one year, whereas only 30% of those who continue their medications will experience a relapse in the same time period (Di Capite et al.). It is widely accepted that genetics play a role in schizophrenia development, but there is no single gene that has been found to be responsible for this disorder. However, some genes have acquired prominent attention in their possible contribution. Dr. Daniel Weinberger, Director of the Genes, Cognition, and Psychosis Program at the National Institute of Mental Health has highlighted the significance of the ​comt gene. ​Mutations in ​comt​ have been found to result in depletion of the critical neurotransmitter dopamine in the frontal lobe (McGrath 2005). A common byproduct of depleted dopamine is hallucinations and delusions which are symptoms of schizophrenia.


Neuroplasticity is the brain’s ability to reform and organize synaptic connections. Neuroplasticity also includes reductions in synapses resulting in a reduction of synaptic strength and pruning axons that are not in use. Events like learning, injury, or stress can help develop and strengthen preexisting neuron pathways or lead to the breakdown of pathways (McEwen et. al. 2016). Experience-dependent plasticity is when certain skills are learned and practiced, leading to a greater part of the brain being connected to the learned skill. In this process there are many neuronal-level changes, such as dendritic spine growth, synaptogenesis, and axon arborization (Diering et. al. 2014). These changes in neuroplasticity have been shown to affect schizophrenia in multiple ways.

Neurobehavior and Schizophrenia

Schizophrenia is associated with functional changes in the cortex. It has been found that neurons in some schizophrenic patients fire more frequently due to an increased sensitivity to excitatory signals, while in others, neurons are unable to appropriately return to their hyper-polarization state (Freeman 2010). This may contribute to schizophrenia patient’s seizures due to rapid over-firing of neurons. Michael Merzenich has started working on brain training software to help schizophrenics. Through the usage of plasticity assisted cognitive remediation (PACR), Merzenich has been using schizophrenic humans and analyzing their visual and auditory fields. By using monkeys, Merzenich has shown how neurons can switch where they receive sensory input from, in this case, the sensory neurons from the damaged hand of a monkey no longer process in the same hand, but process in the healthy hand (Hayden 2015). He used this to connect to his studies in humans, where the visual and auditory fields can still be functional even with damage in certain areas. This was a finding that helped support the claim that neuroplasticity plays an important role in how the brain reacts to stimuli such as an injury. (Hayden 2015). In the past, there have been many experiments conducted as an attempt to find the source of the link between schizophrenia and neuroplasticity. One experiment conducted in 2010 contained 32 stable schizophrenia patients who were placed in one of three cognitive training groups to assess the program’s impact on neurocognition after 6 months. Group one consisted of 12 patients that underwent 50 hours of auditory training. Group two included 10 patients that received an additional 50 hours of visual training and cognitive tasks beyond the 50 hours of auditory training. The third group, a control of 10 patients, underwent 50 hours of computer game tasks. These tasks were performed over a 6-month period and patients were then measured to see if there was any change in their neurocognition. Neurocognition is defined as the functions related to the output of certain parts of the brain. Neuroplasticity is measured by using neurocognition as a reference. At the end of the trial, the 22 patients in the cognitive training group with 50 hours of work experienced significant changes in their processing speed and cognition, but no significant changes were seen in their functional outcomes (Fisher et. al. 2010). However, the patients in the cognitive training group with 100 hours auditory and visual training with cognitive tasks showed significant gains in their cognitive control and memory.

Schizophrenia and Drug Abuse

The three most common drugs used by schizophrenics are nicotine, cannabis, and cocaine (Winklbaur et. al. 2006). These drugs have very detrimental effects in schizophrenics and have the potential to increase symptoms (Ebner 2008).

Nicotine affects patients with schizophrenia in a multitude of ways; the key concern is the impact nicotine has on dopamine and glutamate pathways. Almost 70% of patients that deal with chronic schizophrenia are addicted to nicotine (Winklbaur et. al 2006). Cigarette smoking was also found to have a close link to schizophrenia as well as other mental disorders. Smokers with disorders tend to be more heavily addicted to nicotine and are much less likely to quit smoking than a smoker without a disability (Quigley 2016). There are multiple proposed explanations for the connections between smoking and schizophrenia but there hasn’t been one clear-cut answer. The main ingredient of tobacco smoke is nicotine, which is responsible for the addictive properties of cigarettes. Nicotine travels quickly through the bloodstream and reaches the brain around 15 seconds after being inhaled. Nicotine binds to presynaptic receptors called “nicotinic acetylcholine receptors” located throughout the brain. When the nicotine binds to these receptors, it causes an ion channel to open and release cations through the cellular membrane. These cations – sodium, calcium, and potassium – activate calcium channels and in turn release neurotransmitters. Nicotine changes the release of multiple neurotransmitters – serotonin, GABA, dopamine, and acetylcholine, just to name a few. Elevated acetylcholine levels can result in depression and excess GABA can impair cognitive function (Volk 2018). Increased dopamine is also associated with schizophrenia as many schizophrenics have been found to have this neurotransmitter surplus causing delusions and an altered state of reality (MacCabe 2005).

Cannabis use has been found to be a stressor causing relapse in patients with schizophrenia (Hall et. al. 2008). In a study conducted over 15 years with Swedish participants, it was found that by the age of 18, individuals using cannabis were 2.4 times more likely to be diagnosed with schizophrenia than those who had not used cannabis (Hall et. al. 2008). The increase of the risk of developing schizophrenia directly correlated with an increase of frequency of cannabis usage. In longitudinal studies done by Hall ​et. al.​ it has been shown that cannabis use contributes to schizophrenia through regular use over long periods of time compared to non-users (Hall et. al.). There is also a lot of support for the belief that the connection between cannabis and psychosis, a symptom of schizophrenia, is biologically based (Manseau et. al. 2018). It has been found that in patients with schizophrenia there are elevated levels of anandamide, an endogenous cannabinoid agonist, in their cerebrospinal fluid (CSF) (Manseau et. al. 2018). This highlights a critical link between cannabis and schizophrenia associated symptoms of psychosis. Cocaine is another addictive drug that is commonly abused by schizophrenics. Schizophrenics that frequently use cocaine are at a higher risk for suicidal behavior, tend to be less consistent with their treatments, and are more often hospitalized than schizophrenics who do not use cocaine (Winklbaur 2006). Cocaine has a devastating effect on the neurobiological system, through disruption in reuptake of dopamine in presynaptic receptors (Verma 2015). This causes the dopamine to persist in the synaptic cleft leading to detrimental side effects in schizophrenics such as delirium (Kwak et. al. 2010). Drug abuse can affect neuroplasticity in the brain in multiple ways, depending on the narcotic that is used. There is a possibility that in controlled settings, drug usage may be helpful to schizophrenics as specified doses could possibly alleviate symptoms (Ebner 2008). Overall, there is no clear impact that drug abuse has on the neuroplasticity of schizophrenics, but this is continued to be researched through multiple ongoing clinical trials.


So far, a correlational connection between neuroplasticity and schizophrenia has been formed, but there is a lot of room for determining causation. It has been shown that training leading to an increase in neuroplasticity is associated with a decrease in schizophrenic-like behavior and methods such as cognitive remediation also helps decrease schizophrenic behavior (Mogami 2018). It has been shown that compared to healthy patients, patients with schizophrenia have a lot less neuroplasticity (Jahshan 2017). Factors influencing drug abuse may represent co-morbidities in schizophrenic patients, such as stress. Stress can be a contributing factor in initiation of drug abuse and is associated with many of the symptoms of schizophrenia. Genetic vulnerability also plays a role in drug abuse as many environmental and genetic factors can affect the development of drug addiction. A pressing question of the relationship between schizophrenia and drug abuse is – if schizophrenia onset is associated with drug abuse, is this the result of neuroplasticity increasing or decreasing? Schizophrenia has been hypothesized to affect the reward centers in our brains which increases vulnerability to drug addictions as well. Neurotransmitters are also significant in this process as the intake of certain drugs leads to an excess of dopamine for example, leading to euphoria and hallucinations (Kwak et. al. 2010). Ultimately, the question if drug abuse can cause direct changes to neuroplasticity and therefore schizophrenia still stands. However, there are clinical trials being run to try and elucidate the role of drug abuse manipulation in schizophrenic patients for a beneficial clinical impact (Winklbaur 2006).

Isha Nambisan, Youth Medical Journal 2020


  1. Administrator. “Schizophrenia – Fact Sheet.” ​Treatment Advocacy Center​, nia-fact-sheet#:~:text=Schizophrenia%20is%20a%20chronic%20and%20severe%20neurol ogical%20brain%20disorder%20estimated,untreated%20in%20any%20given%20year.
  2. Begley, Sharon. “Neuroplasticity May Help Schizophrenics.” ​Newsweek​, Newsweek, 13 Mar. 2010,
  3. Capite, Suzanne Di, et al. “The Relapse Rate and Predictors of Relapse in Patients with First-Episode Psychosis Following Discontinuation of Antipsychotic Medication.” ​Wiley Online Library​, John Wiley & Sons, Ltd, 13 Oct. 2016,
  4. “Disorders of Synaptic Plasticity and Schizophrenia.” ​Google Books,​ Google, ophrenia%2Bneuroplasticity&ots=RCU6Z1V6xL&sig=4xPy6QEFnHu7Bf8s18GNnctvW L0#v=onepage&q&f=false.
  5. Fisher, Melissa, et al. “Neuroplasticity-Based Cognitive Training in Schizophrenia: an Interim Report on the Effects 6 Months Later.” ​Schizophrenia Bulletin​, Oxford University Press, July 2010,
  6. Hall, Wayne, and Louisa Degenhardt. “Cannabis Use and the Risk of Developing a Psychotic Disorder.” ​World Psychiatry : Official Journal of the World Psychiatric Association (WPA)​, Masson Italy, 2008,
  7. Howes, Oliver, et al. “Glutamate and Dopamine in Schizophrenia: an Update for the 21st Century.” ​Journal of Psychopharmacology (Oxford, England)​, U.S. National Library of Medicine, Feb. 2015,
  8. Jahshan, Carol, et al. “Enhancing Neuroplasticity to Augment Cognitive Remediation in Schizophrenia.” ​Frontiers​, Frontiers, 15 Sept. 2017,
  9. Karlsgodt, Katherine H, et al. “Structural and Functional Brain Abnormalities in Schizophrenia.” ​Current Directions in Psychological Science,​ U.S. National Library of Medicine, Aug. 2010,
  10. Lodish, Harvey. “The Action Potential and Conduction of Electric Impulses.” ​Molecular Cell Biology. 4th Edition.,​ U.S. National Library of Medicine, 1 Jan. 1970,
  11. Lyon, Edward R., et al. “A Review of the Effects of Nicotine on Schizophrenia and Antipsychotic Medications.” ​Psychiatric Services​, 1 Oct. 1999,
  12. McGrath, John J. “Variations in the Incidence of Schizophrenia: Data Versus Dogma.” OUP Academic​, Oxford University Press, 31 Aug. 2005,
  13. Mogami, Tamiko. “Cognitive Remediation for Schizophrenia with Focus on NEAR.” Frontiers in Psychiatry​, Frontiers Media S.A., 17 Jan. 2018,
  14. NHS Choices​, NHS,
  15. O’Brien, Charles P. “Neuroplasticity in Addictive Disorders.” ​Dialogues in Clinical Neuroscience​, Les Laboratoires Servier, 2009,
  16. Quigley, Harriet, and James H MacCabe. “The Relationship between Nicotine and Psychosis.” ​Therapeutic Advances in Psychopharmacology,​ SAGE Publications, 1 July 2019,
  17. “Researchers Find Way to Increase Neuroplasticity and Treat ‘Negative’ Symptoms of Schizophrenia.” ​Brain & Behavior Research Foundation,​ 15 Aug. 2019, E2%80%9Cnegative%E2%80%9D-symptoms-schizophrenia.
  18. Salleh, Mohd Razali. “The Genetics of Schizophrenia.” ​The Malaysian Journal of Medical Sciences : MJMS,​ Penerbit Universiti Sains Malaysia, July 2004,
  19. – Schizophrenia Genetics and Heredity,​
  20. “Schizophrenia.” ​Mayo Clinic​, Mayo Foundation for Medical Education and Research, 7 Jan. 2020,
  21. “Schizophrenia.” ​National Institute of Mental Health,​ U.S. Department of Health and Human Services,
  22. “Schizophrenia.” ​National Institute of Mental Health,​ U.S. Department of Health and Human Services,
  23. “Treating Schizophrenia: Game On.” ​Nature News,​ Nature Publishing Group,
  24. Vaillancourt, David E, et al. “Dopamine Overdose Hypothesis: Evidence and Clinical Implications.” ​Movement Disorders : Official Journal of the Movement Disorder Society​, U.S. National Library of Medicine, Dec. 2013,
  25. Verma, Vivek. “Classic Studies on the Interaction of Cocaine and the Dopamine Transporter.” ​Clinical Psychopharmacology and Neuroscience : the Official Scientific Journal of the Korean College of Neuropsychopharmacology​, Korean College of Neuropsychopharmacology, 31 Dec. 2015,
  26. Volk, David W, and David A Lewis. “GABA Targets for the Treatment of Cognitive Dysfunction in Schizophrenia.” ​Current Neuropharmacology​, U.S. National Library of Medicine, Jan. 2005,
  27. “What Is Neuroplasticity? A Psychologist Explains [+14 Exercises].”​, 28 Apr. 2020,
  28. Winklbaur, Bernadette, et al. “Substance Abuse in Patients with Schizophrenia.” ​Dialogues in Clinical Neuroscience​, Les Laboratoires Servier, 2006,


The Neuroscience Behind Hiccups


The quick gaps of air, amid a barrage of hiccups, is something that almost all of us can relate to. Derived from the Latin word ‘singult’, that means ‘to catch one’s breath while sobbing’.  Hiccups are defined as the involuntary contractions of the diaphragm followed by the abrupt closure of the trachea, creating a ‘hic’ sound.  And while in evolution, hiccups haven’t been found to hold any significant value to survival, little is actually known about its pathophysiology, and what is its purpose. 


Hiccups are clinically classified by duration, and can be divided into multiple categories:

  • Transient hiccups – A few minutes or seconds
  • Acute hiccups – Less than 48hrs
  • Persistent – Over 2 days
  • Intractable – Over a month
  • Idiopathic chronic hiccup (aka Diabolic hiccup) – recurring hiccup attacks over 1 month

While there haven’t been any big studies on the average duration of hiccups, most hiccups are transient and go unreported. The National Health Service in the United Kingdom says that hiccups should typically last a few minutes but it really varies from person to person.

Hiccups can be onset for a variety of reasons, laughter being one of the most common reasons. Other factors include extreme emotions (e.g. anxiety, stress and excitement), a sudden change in temperature,  eating and drinking too fast, spicy food,  drinking carbonated beverages or too much alcohol.  Hiccups may also be caused by brain tumours, vascular disorders or nerve damage. Sometimes hiccups can also be a symptom of an underlying medical disease such as -Parkinson’s Disease, strokes and ischemia.  


Whilst the mechanism behind hiccups isn’t fully understood, researchers have concluded that there is a neurological reflex arc associated with hiccups.  The reflex arc primarily consists of two parts: the vagus nerve, and the phrenic nerves sending signals from the brain to the diaphragm.  The vagus nerve extends from the medulla to the abdomen, and it conveys innate sensory signals that naturally fire in our CNS.  The phrenic nerves send these signals and electrical impulses from the brain to the diaphragm and intercostal muscles.  The neurological mechanisms behind hiccups are still very poorly understood thus for now is not concrete as it may not only be confined to the medulla but may also involve other parts of the central nervous system (CNS) located between the brainstem and spine.  Researchers assume that patients with chronic hiccuping are likely to have irritation involving this reflex arc such as signals being sent at the wrong times.  Neurotransmitters involved in the process of hiccup have so far been found to include dopamine) and gamma-aminobutyric acid (GABA).  This has been demonstrated as some psychiatric medications that are used to stabilise or modify levels of dopamine and GABA have been found to induce hiccuping.  An example would be Aripiprazole, which is used to stabilize dopamine and serotonin systems through dopamine receptors as well as baclofen, a GABA derivative, which is used to treat hiccup due to CNS tumours and chronic renal failure.

Newborns and infants are particularly prone to hiccups, as they spend roughly 15 minutes a day hiccuping.  Hiccups begin in the womb at around nine weeks.  Researchers found that contractions of the diaphragm from a hiccup triggers two large brain waves followed by a third.  Researchers suppose that as a baby hiccups, the brain may associate the sound of hiccups with the feel of the diaphragm contraction. Being one of the first processes for an infant to experience, a study by Whitehall et al. suggests that hiccuping is significant in the early development of multi-sensory brain connections and signalling.

Parkinson’s Disease

In one study twenty percent of parkinsonism (PD) patients had frequent hiccups. Even in some patients, PD was diagnosed after the occurrence of intractable hiccups. Replacement therapy with dopamine agonists in PD patients is considered to induce certain episodes of a hiccup, however, in others, hiccup may occur as the non-motor symptom of PD rather than a side effect of anti-PD treatment. The pathogenesis is believed to be related to the fact that dopamine agonists share a high affinity for dopamine receptors which may be involved in the hiccup reflex arc.  The drugs to block dopaminergic neurotransmission including chlorpromazine and metoclopramide may be employed in treating hiccup episodes

Treatments for Chronic Hiccuping

Many interventions and nonclinical “cures” for hiccuping have been passed down by word of mouth and experience such as breathing into a bag, holding breath, swallowing granulated sugar, drinking/gargling iced water, forceful traction of the tongue, biting lemon,, eyeball compression, fright etc.  While these remedies can be very convenient and less hazardous, their effectiveness to treat serious hiccups is highly questionable.

For example, gag reflex has long been used as an immediate remedy to treat hiccup.  A possible method of “curing” hiccups could include the regulation of rhythm at which the phrenic nerve operates.

Typically, in the clinical setting, hiccups are not usually the problem itself but is rather a symptom of an underlying problem, thus most cures targeting the root cause of hiccuping such as prokinetics being widely used to treat hiccups due to stomach distension.  Chlorpromazine is currently the only medication approved for hiccups by the US Food and Drug Administration, and for many years it was the primary drug used to treat hiccups.  It acts by targeting dopamine within the hypothalamus.  It has serious potential side effects, including that of- hypotension, urinary retention, glaucoma, and delirium. Initially used to control seizures in patients with epilepsy, vagus nerve stimulators are also the only piece of equipment approved by the FDA for treating hiccups. It sends rhythmic electrical impulses from the brain to the vagus nerve, which passes through the neck, within the reflex arc behind hiccups.  Even a left vagal blockade via nerve stimulation might be applied to stroke-related intractable hiccup after the failure of the phrenic nerve block.


Hiccups for the most part aren’t to be intimidated of, in fact are typically rather humorous.  But as with anything, too much of something can be indicative of much more going on behind the scenes, and this can be particularly applied with hiccups.  A lot of us will look past hiccuping for 5 minutes or so, and cure them with natural or remedies that we’ve tried and tested by past experiences, however,  for those that suffer from such a ‘comedic’ symptom and problem that is chronic hiccuping, there are, but still lacking, drugs and technologies out there that can hopefully help treat this issue.

Nara Ito, Youth Medical Journal 2020


Chang, F. Y., & Lu, C. L. (2012). Hiccup: mystery, nature and treatment. Journal of neurogastroenterology and motility, 18(2), 123–130.

Mayo Clinic. (2017, May 24). Hiccups – Symptoms and causes

Genetic and Rare Diseases Information Center. (2020, 11 5). Chronic Hiccups.

Woelk C. J. (2011). Managing hiccups. Canadian family physician Medecin de famille canadien, 57(6), 672–e201.

Moretto, E. N., Wee, B., Wiffen, P. J., & Murchison, A. G. (2013). Interventions for treating persistent and intractable hiccups in adults. The Cochrane database of systematic reviews, 2013(1), CD008768.

Kohse, E. K., Hollmann, M. W., Bardenheuer, H. J., & Kessler, J. (2017). Chronic Hiccups: An Underestimated Problem. Anesthesia and analgesia, 125(4), 1169–1183.

Whitehead, K., Jones, L., Laudiano-Dray, M. P., Meek, J., & Fabrizi, L. (2019). Event-related potentials following contraction of respiratory muscles in pre-term and full-term infants. Clinical Neurophysiology, 130(12), 2216-2221.


Sleep Restriction Relating to Anger


Anger. One of the most painful emotions to encounter. Regardless of how much humans despise the feeling, everyone has experienced it. Not only is the feeling unpleasant, but the physical and mental health problems caused by excessive anger are dangerous and sometimes even life-threatening. Controlling it is challenging and tedious; allowing it to roam free hurts others and oneself. However, what if there was a way to lessen the amount of anger that is felt by merely sleeping?

A typical person needs 7-8 hours of sleep per night. When getting less than that, one goes into sleep deprivation. When this continues to happen for multiple consecutive days, a person will go into sleep debt. Sleep deprivation and sleep debt are very dangerous for the body because it can cause memory issues, mood changes, weakened immunity, higher risk for diabetes, weight gain, and more. Humans tend to be more irritable when tired. Therefore, it is much more likely for someone to get angry when they are on low sleep. Studies have shown that sleep deprivation can be fuel for anger, and getting enough sleep can lessen the emotion in your body.


In a 2016 study done on 2767 adolescents between the ages of 12 and 16; 52% of the participants were male, and 48% were female. The main objective of this study was to see whether less sleep leads to more behavioral problems. The study showed that the teenagers who slept less had more behavioral problems than those who slept the recommended hours. They reported emotional changes, including an increase in anger.

Another study was done on Japanese high school juniors and seniors to see whether poor sleep habits impacted impulsivity as well as negative behaviors. Teenagers were asked about their sleep patterns; 12% of younger teens and 18% of older teens slept less than the recommended time. These children reported more behavioral issues and negative behaviors/emotions, such as anger. This study helps to prove the theory of sleep deprivation relating to anger.

Furthermore, the amygdala is commonly known as the emotional center of the brain. However, it also plays a crucial role in the process of sleeping. When one is sleep-deprived, there is a functional deficit between the amygdala and the ventral anterior cingulate cortex (VACC), which causes an increase in negative emotions. 


Better sleep will give one a balanced mind. It is evident that sleep and emotions will be correlated because of the functions of the amygdala. The study on adolescents proves that less sleep affects emotions and behavior. Along with this, the Japanese survey of juniors and seniors showed the same results. The less sleep one has, the more likely it is for them to be angry or frustrated throughout the day. Therefore, sleep restriction will increase anger levels.


The Inferior Temporal Cortex “Recycled” to Aid Reading


One of the many strengths of humans is the ability to create and understand intricate languages of reading and writing. Scientists have long debated how humans’ brains have developed these reading and writing specific skills in such a short time.  Neuroscientists’ recent study from Massachusetts Institute of Technology, however, has unveiled that rather than our brains evolving to perform linguistic functions, the inferior temporal cortex (IT cortex) has been “recycled”.  In functional magnetic resonance imaging (fMRI) research, a region within the IT cortex known as the visual word form area (VWFA) lightens when the brain recognizes orthographic stimuli, in this case, words.  Additionally, researchers used fMRI to find that areas of the IT cortex meant for face and object recognition lit up distinguishing words after learning to read. This shows that the human mind is adaptable and can repurpose itself for different tasks, and in this case, for reading.


To test this theory, Old-World monkeys, such as baboons and rhesus macaques, which diverged from humans about 25 million years ago, were studied.  Despite not being perfect models for the human mind, these primates have enough similarities to be comparable.  Research has shown that we share similar functions and structures in the ventral visual pathway which is a section of the brain utilized for object recognition. In prior research from 2012, baboons were able to differentiate real English words and nonsensical combinations of letters or non-words with enough training.  This proves that word recognition is something that does not require years of evolution and a complex understanding of linguistics.  However, researchers still pondered the neural workings behind this skill.  

This curiosity led to a new test, where scientists used microelectrode arrays to record the neural activity in untrained macaque monkeys while they examined both words and non-words.  These arrays were placed in the monkeys’ IT cortex as well as a part of their visual cortex called V4, which connects to the IT cortex.  Then, they put the data into a linear classifier, a computer model designed to identify whether or not words triggered neural activity in the monkeys.  Dr. Rishi Rajalingham, the lead of this study, explained that this process is very effective and easy, because there is no training necessary for the monkeys.  


In this diagram, Model A presents an example of text the macaque monkeys would view, a visual of the IT cortex, and V4 lighting up.  On the right, the figure shows which orthographic tests affect which specific neurons using data from the microelectrode arrays.

Model B displays three different sets for the monkeys.  The first contains samples of words and random assortments of letters, and the second tests the variation in the size and spacing of the words. The third set displays one letter but each card has the letter in different locations.  

Model C presents the location of the microelectrode arrays in 4 example monkeys: N, S, B, and M.  To the right are 8 different graphs representing example IT sites, each with some of the monkeys’ neuronal response to a set of 5, consisting of both words and a random string of letters.  The colors of the data show the intensity of the response with blue being the lowest and red being the highest.  In addition, there is shading around some sections of the data that represents the general margin of error.  Over the 300 millisecond time frame, many of the words sparked higher responses in the monkeys compared to the jumbled letters despite having no prior training or experience with orthographic stimuli.  

The model displayed that the data corresponding to the IT cortex was about 70% accurate, with both performance and errors made by these monkeys similar to the baboon study in 2012.  Meanwhile, the visual cortex was notably less accurate which reveals that the skilled areas of the IT cortex for object recognition are specifically capable of being remodeled if needed for reading.  These observations reveal that the IT cortex in untrained monkeys is sufficient enough to complete simple orthographic tasks such as word recognition.  In the future, researchers plan on studying both trained monkeys and literate humans to compare results. With adequate training, our brains are capable of learning to read without highly evolved brains and by “recycling” our IT cortex.


The inferior temporal cortex is a potential cortical precursor of orthographic processing in untrained monkeys, Nature Communications, August 2020

“Parts of the human brain have been ‘recycled’ for reading, indicates study”, News Medical Life Sciences, August 2020

“To read, humans ‘recycled’ a brain region meant for recognizing objects”, United Press International, August 2020

“Key brain region was ‘recycled’ as humans developed the ability to read.”, MIT News, August 2020

Orthographic Processing in Baboons (Papio papio), Science, April 2012

Kyle Phong, Youth Medical Journal 2020