Categories
Neuroscience

An Overview of Memory and Amnesia

Introduction

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.

Conclusion

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

References

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.

Categories
Neuroscience

The Link Between Schizophrenia and Neuroplasticity

Introduction

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

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.

Conclusion

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

References

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Categories
Neuroscience

The Neuroscience Behind Hiccups

Abstract

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. 

Background

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.  

Causes

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.

Conclusion

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

References

Chang, F. Y., & Lu, C. L. (2012). Hiccup: mystery, nature and treatment. Journal of neurogastroenterology and motility, 18(2), 123–130. https://doi.org/10.5056/jnm.2012.18.2.123

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

https://www.mayoclinic.org/diseases-conditions/hiccups/symptoms-causes/syc-20352613

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

https://rarediseases.info.nih.gov/diseases/6657/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. https://doi.org/10.1002/14651858.CD008768.pub2

Kohse, E. K., Hollmann, M. W., Bardenheuer, H. J., & Kessler, J. (2017). Chronic Hiccups: An Underestimated Problem. Anesthesia and analgesia, 125(4), 1169–1183. https://doi.org/10.1213/ANE.0000000000002289

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.

Categories
Neuroscience

Sleep Restriction Relating to Anger

Introduction

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.

Studies

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. 

Conclusion

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.

Categories
Neuroscience

The Inferior Temporal Cortex “Recycled” to Aid Reading

Abstract

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.

Experiment

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.  

Data

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.

References

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

https://www.nature.com/articles/s41467-020-17714-3

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

https://www.news-medical.net/news/20200805/Parts-of-the-human-brain-have-been-e2809crecyclede2809d-for-reading-indicates-study.aspx

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

https://www.upi.com/Science_News/2020/08/04/To-read-humans-recycled-a-brain-region-meant-for-recognizing-objects/8801596564675/

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

http://news.mit.edu/2020/brain-recycled-ability-read-0804

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

https://science.sciencemag.org/content/336/6078/245.abstract

Kyle Phong, Youth Medical Journal 2020

Categories
Neuroscience

An Outlook Into Society and Medicine Through A Neurological Disease

Cause, Symptoms, and Diagnosis

Anti-NMDAR encephalitis is a rare neurological autoimmune disease that can cause severe symptoms [1]. In brief, autoimmune disorders can be simplified as the immune system attacking the body [2]. For this disorder, the immune system has created antibodies against the NMDA receptors, which are responsible for learning, judgment, and autonomic activities like breathing or swallowing. Still, the cause is unknown [3].However, anti-NMDAR encephalitis appears linked to tumors, especially ovarian tumors [4]. In addition, cases appear to occur after a viral infection, especially herpes simplex virus [5]. `

For neurological symptoms, this can include unconscious movement, memory issues, and damage to cognition. However, psychiatric symptoms are more clear from onset. Consequently, anti-NMDAR is often misdiagnosed as a psychiatric disorder. These severe symptoms include paranoia, delusions, and psychosis [1]. Recovery can range from months to years but has improved with the development of immunotherapies [3]. 

Typically, physicians will recognize these symptoms first and then order testing. This involves testing the blood serum or cerebral spinal fluid for NMDAR antibodies [1]. Besides that, additional testing can be done to detect symptoms. This usually includes tumor imaging, an MRI, or an electroencephalogram (EEG) [3]. Still, first-line doctors like emergency physicians or primary care providers often misdiagnose anti-NMDAR encephalitis as a psychiatric disorder because of its symptoms. Its strong prevalence in women, as approximately 80% of patients are female, also causes misdiagnoses. There is no clear marker, so physicians must be familiar with the myriad of symptoms involved in order to identify it [5].

Figure 1. The MRI of a male with anti-NMDA receptor encephalitis, his MRI after treatment, and the MRI of a health volunteer [4].

Treatment and Prognosis

Patients with the best prognosis have typically had a tumor removed, are young, or have a low concentration of antibodies in their blood serum or cerebral spinal fluid. This usually results in substantial improvement. Conversely, patients who did not have a tumor typically have worse outcomes [5]. The length of recovery can range from months to years, depending on severity and treatment. Early diagnosis and treatment is directly correlated with improved outcomes [3]. However, anti-NMDAR encephalitis is frequently misdiagnosed due to the preponderance of severe psychiatric symptoms. This can hinder a patient’s recovery [5]. Other than removing the tumor, patients can receive steroids or immunosuppressants to weaken the antibodies that are attacking the body [1]. After receiving treatment, outcomes are acceptable. The symptoms subside in the order that they occurred, typically beginning with the most severe issues. Still, some patients continue to experience memory and cognition issues. In the worst of cases, anti-NMDAR encephalitis is lethal, killing approximately 6% of patients[4]. 

A Dark History for Women

From Ancient Greece, hysteria has been a common diagnosis for women experiencing psychiatric issues, essentially attributing their issues to their gender. However, some scientists propose that there is a logical explanation for this misdiagnosis. Specifically, that explanation is anti-NMDAR encephalitis. This disease predominantly affects women and also causes severe psychiatric symptoms.

Additionally, the removal of ovarian tumors is one of the most effective treatments for the disease [6]. From antiquity, a treatment for hysteria and other health issues in women has been sterilization by removal of the reproductive organs. In removing the reproductive organs, tumors are also excised. One such operation was created by the surgeon Robert Battey, and he referred to it as the “normal ovariotomy”. Originally, this was to treat menstrual disorders and other symptoms. Later on, it was used to treat psychiatric and neurological disorders in women, often without their consent. Even so, surgeons and their communities accepted this, because the patients generally improved. [7]. 

Additionally, other scientists speculate that anti-NMDAR encephalitis is responsible for historical reports of “demonic possession”.  One of the symptoms are sudden, “jerking” movements of the limbs that are entirely unconscious. In addition, a common psychiatric symptom is paranoid delusions of danger. This appears congruent with descriptions of possession. Once again, because anti-NMDAR encephalitis patients are primarily women, it may have led to the misconception that this gender is weaker and therefore more susceptible to the supernatural or witchcraft [8].

Modern Social Implications

Anti-NMDAR encephalitis is a newly discovered disease, only described in 2007 by Dr. Josep Dalmau at the University of Pennsylvania [9]. Because of its severe symptoms and historical linkage, this led to introspection into the role of women in healthcare. 

Much has changed since Battey’s ovariectomies, but women continue to experience issues in medicine. From the perspective of a patient, some women fail to receive psychiatric treatment, because these issues are considered “normal” for their gender. For anti-NMDAR encephalitis in particular, neurologists voice concerns that their patients cannot receive treatment or will be misdiagnosed with a psychiatric disorder. Some diagnoses include insanity or psychosis, whose treatment still includes electroconvulsive therapy. In essence, patients with those misdiagnoses would receive improper care. Rapid diagnosis and treatment are especially important in recovery, but this is hindered by gender issues [8].

One woman voiced her story in the 2012 novel Brain on Fire: My Month of Madness. The author and career journalist, Susannah Cahalan, contracted anti-NMDAR encephalitis only three years after it was discovered. At the time, her doctor estimated that only ten percent were correctly diagnosed. In her personal stories, Cahalan’s doctors grossly misdiagnosed her, ranging from “parties to much” to bipolar disorder. After a few months and the onset of severe neurological symptoms, she was finally diagnosed with anti-NMDAR encephalitis. Her best-selling novel and subsequent has made anti-NMDAR encephalitis one of the more famous neurological diseases. Now, diagnosis is often faster and treatment has improved [10].

Final Words

Anti-NMDAR encephalitis has an innate link between science, medicine, the media, and society. Specifically, it outlines the path of a disease, from its discovery in science, applications in medicine, coverage by the media, then perception in society. The concern for women and their mental health has not stopped, but it has been ameliorated in the case of anti-NMDAR encephalitis, where patients can get diagnosed quickly enough to have an optimal prognosis. Nonetheless, it is vital that the healthcare industry utilizes the media effectively to advocate for its patients.

References

[1] Anti-NMDAR Encephalitis. Perelman School of Medicine. https://www.med.upenn.edu/autoimmuneneurology/nmdar-encephalitis.html.

[2] Irani, Sarosh and John Radcliffe. NMDAR Antibody Encephalitis. Encephalitis Society. https://www.encephalitis.info/nmdar-antibody-encephalitis.

[3] What is Anti-NMDA Receptor Encephalitis?. The Anti-NMDA Receptor Encephalitis Foundation. https://www.antinmdafoundation.org/the-illness/what-is-anti-nmda-receptor-encephalitis/

[4]  Hughes, Ethan G., et al. (2010). Cellular and Synaptic Mechanisms of Anti-NMDA Receptor Encephalitis. Journal of Neuroscience. 30. https://dx.doi.org/10.1523%2FJNEUROSCI.0167-10.2010 

[5] Chanaka, Amugoda, et al. (2019). Anti-NMDAR Encephalitis: Higher Suspicious Needed for Earlier Diagnosis. Hindawi. https://doi.org/10.1155/2019/7476254 

[6] Pollak, Thomas A. (2013). Hysteria, hysterectomy, and anti-NMDA receptor encephalitis: a modern perspective on an infamous chapter in medicine. British Medical Journal. 346. https://doi.org/10.1136/bmj.f3756 

[7] Komagamine, Tomoko, et al. (2019). Battey’s operation as a treatment for hysteria: a review of a series of cases in the nineteenth century. History of Psychiatry. 55-66. https://doi.org/10.1177/0957154×19877145 

[8] Radecki, Ryan P. (2019). Demonic Possession or Autoantibody-Mediated Encephalitis?. ACEP Now. https://www.acepnow.com/article/demonic-possession-or-autoantibody-mediated-encephalitis/

[9] Dalmau, Josep. (2007). Paraneoplastic anti–N‐methyl‐D ‐aspartate receptor encephalitis associated with ovarian teratoma. Annals of Neurology. 25-36. https://dx.doi.org/10.1002%2Fana.21050 

[10] Cahalan, Susannah. (2012). Brain on Fire: My Month of Madness. Simon and Schuster. 

Aleicia Zhu, Youth Medical Journal 2020

Categories
Neuroscience

Mental Health: What is Good Life?

The key to happiness and good life has been disputed among many contemporary and past philosophers to search for a finding of these factors. This essay answered this research question: What factors play an important role in the philosophy of a good life? By exploring the factors of gratitude, exercising, and the use of idle time, this essay highlighted and proved that it has a strong impact on emotional and physical health, as well as maintaining happiness in life. Gratitude, for example, allows the brain to release ‘happy chemicals’ that are used to make one feel positive. Exercising, similarly, produces these chemicals that relieve stress and the worrisome of life. Lastly, the use of idle time fuels creativity and improves one’s mental intricacies. The inducement of happiness derived from these factors has been addressed throughout the essay coupled with research such as from experts and professors. Naturally, this essay acknowledges only a myriad of possible interpretations of ways of life, which may challenge the points raised within this essay.

The philosophy of a good life has been challenged by many individuals and philosophers. From Plato to Aristotle, many theories of life such as the moral life where your moral values present as an important factor of happiness in your life,  pleasure life where your pleasure is what makes life worth living, or the meaningful life that argues that to have a good life one has to make their life’s worthy of existence. This essay seeks to universalize the idea of a good life and challenge the theories offered by many Greek philosophers of a good life. For instance, Socrates’ idea of the moral life, Epicurus’ idea of the life of pleasure, and the theory of a meaningful life.   

What factors play in the philosophy of a good life? To explore and answer this theory, this essay will examine the three components to a good life. These include relaxation, exercising, and use of idle time. Using research from the Mental Health Organization, an article by a professor of philosophy at University Dublin, Hallie Smith with the education of a Master’s degree, and a health and lifestyle writer, Markham Heid, this essay will showcase the key factors to life. To further explore these key ideas, this composition will also highlight how these components contribute to your emotional and physical health, and how that will play in the overall happiness in your life. This research question is worthy of research because it is an endearing question that is present throughout ancient Greek history to modern society today. A philosophy of life allows us to guide ourselves to a good life, rather than aimlessly walk through life.In our busy, daily lives we often have instances where we forget about our possessions or thoughts that are important. These happenings occur because of our packed schedules and events that cause us to take away our own time. Often, our work is the basis of our life, as it is the structure that is providing you the necessities for living. This idea is integrated into our modern society and has created a culture where your work dominates a good portion of your lifespan, and where your idle time or free time has been reduced. Hence, a work-centered life restricts your freedom, and while allowing time to idle and not working  “help develop mental processes[,]storage and retrieval”(Heid, “Why Your Brain Needs Idle Time). 

Allowing our thoughts to be free and our creativity to be fueled, downtime is more beneficial than it seems. The ideas that idle time is a waste of productivity and a product of laziness are now manufactured in our fast-paced society; however, idle time is a way to give freedom to your body and it is a self-meditation technique, where it inspires you and allows you find the inner peace within yourself. It is where our minds and body relieve the internal stress and worry of our modern work and the time for our mental intricacies to be enhanced. Therefore, allowing more idle time to be in our lives, relieves more of our liberation to stress and adversity that relentlessly concede in our modern society. 

One of the most unparalleled emotions that humans possess is gratitude. It is the emotion that portrays your moral values and reflects an individual’s character. With gratitude, one can be open-minded towards life and induce happiness and an individual’s healthiness in life. As evident as exercising is beneficial to your health, being grateful has shown to be also instrumental. According to Melanie Greenberg, Ph.D., being able to be grateful is beneficial with regards to “health, happiness, satisfaction with life, and the way we relate” to other people that we coexist with (“How Gratitude leads to A Happier Life”).  With the ability to indicate thankfulness for and to return graciousness, individuals display their kindness, caring, and respect for the world around them. Not only does enacting gratitude impact the ones around an individual, but also, in return, benefit the individuals that act upon it. 

For instance, our brain reacts to gratitude as a positive sign, therefore, we produce good feelings related to how exercising releases endorphins to dull the pain of working out; however, being grateful does not take excessive strength to carry out those happy chemicals, but rather, according to Kaia Roman, author of The Joy Plan, your “optimistic thoughts calm and soothe the amygdala” which is the part of the brain that signals stress (“So This Is Why Gratitude Makes Us Happier”). Optimism is also a crucial benefit from gratitude, it allows individuals to see the world in a different perspective, which helps one realize that sometimes our troubles and worries may not be as significant as the problems that other people in the world are facing. Gratitude inspires positive feelings, such as happiness, life, and fulfillment, which some studies display that it can trump out the pessimistic feelings that an individual might pertain to. By apprehending gratitude, individuals are able to turn our brains in a more optimistic mode, which in return, atones our brain’s proneness to concentrate on menaces, stress, and the nullifying parts of living (Greenberg, “How Gratitude Leads to A Happier Life”). Hence, life becomes fulfilling and the desire to want slowly diminishes as gratitude becomes more normalized. 

According to Melissa Chu, a writer for the Medium, asserts, “Those who were less grateful were more stressed, anxious, and depressed” (Why Gratitude Makes You Happier, Healthier, and More Popular”). Incoherence, the more grateful one is in life, the happier one will become.  For these reasons, gratitude is also integrated with many religions, such as Islam and Christianity, which enforces followers of the religion to have moral values that could help them be successful in life. Being able to have gratitude is also a moral that is well valued in today’s society. It reveals much of an individual’s nature; as a caring and humble character. Expressing and enveloping thoughts of gratitude not only can build a fine personality of an individual, but it can also as well create a more positive spin on a latter situation that allows the individual to deliberate into the optimistic side of life. Therefore, by being grateful, individuals are even able to appreciate the things that make the littlest impact of their life. 

References

  1. Chu, Melissa. “Gratitude Makes You Happier, Healthier, and More Popular.” Ladders, Ladders, 2 Oct. 2019, http://www.theladders.com/career-advice/gratitude-makes-you-happier-healthier-and-more-popular.
  2. Greenberg, Melanie. “How Gratitude Leads to a Happier Life.” Psychology Today, Sussex Publishers, 22 Nov. 2015, http://www.psychologytoday.com/us/blog/the-mindful-self-express/201511/how-gratitude-leads-happier-life.

Heid, Markham. “Why Your Brain Needs Idle Time.” Medium, Elemental, 6 May 2019, https://elemental.medium.com/why-your-brain-needs-idle-time-e5d90b0ef1df

Categories
Neuroscience

Does Personality Affect Genetics?

Creativity, temperament, curiosity, and compassion; these are just some of the pillars of what makes a person who they are. Our actions as human beings are based on personality because we are an emotional species. This emotion drives us and makes up our identity. Therefore, emotions are a result of experiences that mold your character. We must ask the question of whether personality is entirely up to us. Are we the ones driving the car to the path of identity, or is there a map? Does genetics play a role in our personality? Recent studies have shown specific genes in our DNA that significantly affect how our character is shaped.

In 2010, there was a meta-analysis study done on genome-wide lab data for “personality in 10 discovery samples (17,375 adults) and 5 in silicone replication samples (3,292 adults),” (Moor). All people were from European ancestry. Personality was scored for neuroticism (negative emotions), extraversion (positive emotions), openness to experience, agreeableness, and contentiousness. The scoring was all based on the NEO Five-Factor Inventory. “The NEO Five-Factor Inventory-3 (NEO-FFI-3), is the updated version of the NEO-FFI — a 60-item version of the NEO-PI-3. It provides a quick, reliable, and accurate measure of the five domains of personality and is particularly useful when time is limited and when global information on personality is needed”(NEO).

The results were as following:

 “ genome-wide significance to Openness to Experience near the RASA1 gene on 5q14.3 (rs1477268 and rs 2032794, p=2.8*10-8) and for Contentiousness in the brain-expressed KATNAL2 gene on 18q21.1 (rs2576037, P=4.9*10-8). We further conducted a gene-based test that confirmed the association of KATNAL2 to contentiousness. In silico replication did not, however, show significant associations of the top SNPs of Openness and Contentiousness, although the direction of the effect of the KATNAL2 SNP on Contentiousness was consistent in all replication samples,” (Moor).

The data from this study shows that there is a genome-wide significance relating to the RASA1 and KATNAL2 gene to 2 domains of personality. Further research was done on the KATNAL2 gene, associated with the personality domain of contentiousness The effect of the KATNAL2 SNP (single nucleotide polymorphism) showed to be consistent.

Single nucleotide polymorphism: .“Single nucleotide polymorphisms (SNPs) are a type of polymorphism involving variation of a single base pair” (Si Nu Po).

Another study was done on Norwegian twins to estimate how much impact genetics have on our personalities. For this study, scientists used the NEO-PI-R model of the NEO Five-Factor Inventory and the Satisfaction With Life Scale (SWLS).“The Satisfaction with Life Scale was developed to assess satisfaction with people’s lives as a whole. The scale does not assess satisfaction with specific life domains, such as health or finances, but allows subjects to integrate and weigh these domains in whatever way they choose” (Sat). Regression analyses and biometric modeling were used to determine influences on personality traits and where they came from, whether it be genetics or environmental. The results showed that Extraversion and Neuroticism emotions explained 24% of the variance in life satisfaction and facets explained 32%. Out of these facets, four were examined closer to the study. “Anxiety and depression in the Neuroticism domain, and activity and positive emotions within extraversion. Heritability of life satisfaction was 0.31 (0.22–0.40), of which 65% was explained by personality-related genetic influences” (Røysamb). 

In conclusion, though we have control over who we become, some parts of our identity were predetermined at birth. Through research and experimenting, scientists can give us a deeper understanding of this new, unknown topic. The meta-analysis study proved that there was a difference in the KATNAL2 gene when it comes to levels of Contentiousness and in the RASA1 gene with levels of Openness. The twin study showed that 65% of the heritability of life satisfaction came from genetic influences on personality. These two studies came to a similar conclusion; personality is affected by genetics.

References:

Røysamb, Espen, et al. “Genetics, Personality and Wellbeing. A Twin Study of Traits, Facets and Life Satisfaction.” Nature News, Nature Publishing Group, 17 Aug. 2018, http://www.nature.com/articles/s41598-018-29881-x.

Moor, M H M de, et al. “Meta-Analysis of Genome-Wide Association Studies for Personality.” Nature News, Nature Publishing Group, 21 Dec. 2010, http://www.nature.com/articles/mp2010128.

Jaime Derringer, Robert F. Krueger. “Predicting Sensation Seeking From Dopamine Genes: A Candidate-System Approach – Jaime Derringer, Robert F. Krueger, Danielle M. Dick, Scott Saccone, Richard A. Grucza, Arpana Agrawal, Peng Lin, Laura Almasy, Howard J. Edenberg, Tatiana Foroud, John I. Nurnberger, Victor M. Hesselbrock, John R. Kramer, Samuel Kuperman, Bernice Porjesz, Marc A. Schuckit, Laura J. Bierut, , 2010.” SAGE Journals, journals.sagepub.com/doi/10.1177/0956797610380699.

Krueger, Robert F, et al. “The Heritability of Personality Is Not Always 50%: Gene-Environment Interactions and Correlations between Personality and Parenting.” Journal of Personality, U.S. National Library of Medicine, Dec. 2008, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593100/.

“NEO Five-Factor Inventory – 3.” SIGMA Assessment Systems, 20 Dec. 2018, http://www.sigmaassessmentsystems.com/assessments/neo-five-factor-inventory-3/.

“Single Nucleotide Polymorphisms (SNPs).” Genome.gov, http://www.genome.gov/genetics-glossary/Single-Nucleotide-Polymorphisms.
“Satisfaction with Life Scale.” Satisfaction with Life Scale | Positive Psychology Center, ppc.sas.upenn.edu/resources/questionnaires-researchers/satisfaction-life-scale#:~:text=The%20Satisfaction%20with%20Life%20Scale,in%20whatever%20way%20they%20choose.

Categories
Neuroscience

Insight into Human Intelligence

When we talk about intelligence, it is often associated with school smarts or sometimes we reflect this term upon an archetype of an old man. Intelligence, however, is defined, in common psychology, as an intangible object and rather an ability to adapt to new situations , solve problems by learning, mentally assimilating into challenging environments , and overcoming obstacles. Intelligence can take a variety of forms, ranging from spatial, linguistic, intrapersonal, interpersonal, social, to emotional intelligence. This idea aligns with Eric Garner and was brought to attention by other psychologists such as Sternberg and his triadic theory or Spearmen with his g factor theory. Whether you are bad at math or have trouble connecting with others, these theories tell us that areas that you are not particularly advanced at, oftentimes translate into other forms of abilities of which you might not be aware

Biological discoveries of the brain have also made further developments into apprehending human intelligence. For instance, one of the most well-known scientists and theorists, Albert Einstein has rumored to average around a genius, and studies have assumed that Einstein’s brain differed from others in which the components of his neurological composition might have been an imputing factor to his intelligence. This study, conducted by Florida State University evolutionary anthropologist Dean Falk, revealed that the prefrontal cortex of Einstein’s brain, the area for abstract thinking, was inherently different from others in that it contained “unusually complex patterns of convolutions”. This complex design led to another discovery of the abundance of “helping cells”, or glial cells, that may also be a reason for why Einstein was so mentally adept.  

In the intelligence spectrum, like any normal curve distribution, there are sometimes outliers and extremes of the human brain. An IQ below 70, for instance, is considered to be a lower outlier indicating a mental disability, while someone who has an IQ above 140 is seen as a genius. This comparison between one’s mental capacity is often determined by intelligence tests such as the Wechsler Adult Intelligence Scale (WAIS) for adults and the Wechsler Intelligence Scale for Children (WISC) for children and teens. These tests are divided into 10 subtests that inspect one’s verbal, perceptual, reasoning, logic, and memory intelligence. A final score is derived from these tests and is finally compared on a bell-curve scale. 

We would expect IQ, then, to be a factor in the occupations that people have and their requirements for certain jobs. Many studies have shown such evidence of a correlation between IQ and occupations. In fact, a prediction of low IQ and low success is more accurate than a high IQ with high success. We can fairly predict one’s occupational level by referencing an individual’s economic background and their parent’s job holdings. This circumstance is the case where hereditary provides a larger percentage in a person’s intelligence rather than the case where the environment plays the shadowing role. According to recent studies hereditary provides about 80% to intelligence while environmental factors only attribute about 20%. Hereditary, or your parents’ intelligence, therefore, is four times more likely to determine your IQ.

Intelligence tests, however, may not entirely determine your mental capacity or define who you are. For example, in special cases where people who have the savant syndrome -a condition in which a person otherwise limited in mental ability has an exceptional specific skill, such as in math or drawing- exemplify extraordinary abilities that others don’t possess and in which cannot be demonstrated on a simple reading and writing test. Famous savants such as Leslie Lemek suffer from complications at birth, but, like other savants, he shares an incredible talent in music. Insight into special cases like these help renovate IQ tests and aid people in emphasizing and helping them realize their specialty. 

The validity of intelligence tests also comes into question when assessing individuals. An individual’s motivation or persistence, for example, maybe the result of a failed exam rather than his intelligence. This idea is paralleled when approaching how kids and teens take these kinds of tests. Are they actually motivated and focused on the test, or are they finishing it to just get it over with?  IQ tests are then merely reduced to a performance test,  measuring one’s verbal and nonverbal intelligence. Intelligence tests only seem to measure one aspect of an individual, it does not give insight into someone’s anxiety with tests, one’s persistence, or other traits that IQ tests don’t veil. Cultural differences also call for well-established tests and forms of practical tests that are usable for everyone around the world.

References

  1. Bryd, Deborah. “Einstein’s Brain Was Different from Other People’s.” EarthSky, 2012, earthsky.org/human-world/einsteins-brain-was-different-from-other-peoples.

2. Eysenck, H. J. Know Your Own IQ. Penguin, 1962.

3.Black and White Portraits of Famous People, historicalphotographsoftheworld.blogspot.com/p/potraits.html.

4.“Getting Help for a Gambling Addiction.” SpunOut.ie – Ireland’s Youth Information Website, spunout.ie/health/article/gmb-scc-help-for-a-gambling-addiction.

5.“I.Q. Test Information.” Zetnet Meta Refresh, http://www.users.zetnet.co.uk/think/inform.htm.

6. IQTest. “IQ Bell Curve.” IQ Test Prep, 2020, iqtestprep.com/iq-bell-curve/.

Categories
Neuroscience

Glioblastoma: The Deadliest Brain Tumor

Abstract

Glioblastomas (also known as GBM) are the most prevalent form of adult brain tumors, accounting for approximately 78% of all malignant tumors. They are usually very aggressive, which means they  grow rapidly and spread quickly. The following article offers a brief overview of the symptoms, diagnosis, treatment, as well as different types of glioblastomas.

Introduction

Glioblastomas are an aggressive type of cancer that can occur in the brain or spinal cord. They are the rarest type of malignant Grade IV tumor, where a large portion of tumor cells, or astrocytes, reproduce and divide at any given time. These astrocytes are nourished by an ample and abnormal blood vessel supply. While predominantly consisting of abnormal astrocytic cells, the tumor can also contain a mix of different cell types and patches of necrosis, or death of body tissue. These invasive tumors are infiltrative and can spread into nearby regions of the brain, sometimes spreading to the opposite side of the brain through connection fibers in the corpus callosum, the thick band of nerve fibers that divides the cerebral cortex lobes into left and right hemispheres. This aggressive tumor may arise de novo, meaning they begin as a Grade IV tumor with no evidence of a lower grade precursor. De novo tumors are the most common form of glioblastoma, tending to be quite aggressive and more likely to affect older patients. Alternatively, secondary glioblastomas may progress from lower-grade astrocytic tumors and evolve into Grade IV tumors over time. While these tumors tend to grow slowly initially, they can progressively become aggressive. 

Diagnosis and Symptoms

Glioblastomas are generally found in the cerebral hemispheres of the brain, but can be found anywhere in the brain. Patients with glioblastomas develop symptoms rapidly due to mass effect from the tumor itself or from the fluid surrounding the tumor that causes further brain swelling. Common symptoms can be nausea, vomiting, and severe headaches, which are all related to increased pressure in the brain. Patients can also present neurological symptoms that are dependent on the location of the tumor. These symptoms could include weakness in extremities, difficulty balancing, and memory loss. The standard procedure for diagnosing glioblastomas includes a neurological exam, an imaging test, and a tissue biopsy. During the neurological exam, doctors will typically check a patient’s vision, hearing, balance, coordination, strength, and reflexes. This can aid the doctor by providing an idea of where the tumor might be located. Further imaging tests, such as an MRI and fMRI, can determine the location and size of the brain tumor. Finally, the tissue biopsy can be analyzed in a laboratory to determine the type of cells present in the tumor and their aggressiveness. 

Treatment

Glioblastoma can be difficult to treat since some cells may respond well to certain therapies, while others may not be affected at all. Because of this, the treatment plan for glioblastoma may combine several approaches. The first step in treating glioblastoma is a surgical procedure to make a diagnosis, to relieve pressure on the brain, and to safely remove as much tumor as possible. Glioblastomas are diffuse and have finger-like tentacles that infiltrate the brain, which makes them very difficult to remove completely. This is particularly true when the tumors are growing near important regions of the brain that control functions such as language, movement, and coordination. After surgery, radiation or chemotherapy may be used to slow down the growth of the residual tumor after surgery or for tumors that are inoperable. The standard of care treatment for newly diagnosed GBM depends on a variety of factors, including molecular biomarkers and age. Recurrent GBM is treated based on the patient’s response to initial treatments and assessment of disease progression. Other courses of treatments can also include targeted drug therapy, clinical trials, and palliative care.   

Prognosis and Conclusion

Long-term survivors of glioblastoma are rare, with only 6% of patients surviving more than 5 years after initial diagnosis. Several variables besides tumor size and location determine a patient’s survival chances: age at diagnosis, as younger patients often receive more aggressive, multimodal treatment; functional status, which has a significant negative correlation with age; and histologic and genetic markers. Despite advances in surgery, radiation therapy, imaging, and chemotherapy, the median survival for patients with glioblastoma remains dismal. It is a devastating cancer that deserves better therapeutic approaches and translational research, which is achievable with further research.