APRIL 2020 | NEWSLETTER #2
NEUROPSYCHOLOGY
What counts as neuropsychology? Find out by reading!
By Psychology Enthusiasts' Circle Neuropsychological Insights into ADHD 01 Functional Neuroimaging and Depression 04 Neuropsychological Implications of Insomnia 09 Time Perception 15 Neuropsychological Functioning in Bipolar Disorder 18
01
NEUROPSYCHOLOGICAL INSIGHTS INTO ADHD By Jasmine Chan
Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in childhood. In the US alone, around 6.1 million children suffer from it. Children with ADHD are typically impulsive, have poor concentration and high levels of activity, although some are predominantly attention deficit, some hyperactive, and the others a mixture of both. The disorder greatly hinders students’ academic, social and emotional development, and leaves countless parents and schools frustrated.
Attention deficit hyperactivity disorder, otherwise known as ADHD
ADHD is usually diagnosed by mental health professionals or other specialists through procedures like physical assessments, interviews and listening to the reports of significant people such as parents and teachers, with accordance to the guidelines in the American Psychiatric Association’s Diagnostic and Statistical Manual, Fifth edition (DSM-5). However, this psychological method of diagnosis is inevitably subjective as it often includes self-reporting assessments. For instance, if parents believe their child has ADHD and needs medication, they will likely say that he or she can never pay attention and is always overly active, when in reality, it might not be the case. Hence, it is suspected that there are misdiagnoses for the disorder.
02 ADHD misdiagnosis might be attributed to age and sex. Schools sort children into grades according to age, creating an age gap between those at the two ends of the categories, i.e. a child who has just turned five could be in the same grade as one who is almost six, and their age difference is around 20%. This is particularly problematic as diagnoses might take into account the child’s performance relative to their peers instead of his or her actual abilities, yet it is not a fair comparison because their level of development should not be the same. A study even found that boys and girls born in December are 30% and 70% more likely to be diagnosed with ADHD than those born in January respectively. Similarly, sex might have also caused misdiagnoses. Boys are found to be 3 to 9 times more likely to be considered to have ADHD than girls, but if ADHD is a neurodevelopmental disorder, the chance of having it should be equal among the two sexes. This hints that there is a possibility of misdiagnosis. Misdiagnosis contributes to the stigmatization of ADHD. Psychological methods of diagnosis cannot show that ADHD patients are biologically different from those without ADHD because they only evaluate patients’ behaviour, leading some to believe that ADHD is not an actual mental disorder, but an excuse for people to be lazy. It casts a stereotype on ADHD patients, labelling them as academically incompetent, and causes some to lose confidence in their abilities. Additionally, people might believe that ADHD should only occur in boys because currently diagnosed ADHD patients are predominantly male. Girls with ADHD are thought to have something very wrong with them. Therefore, psychology seeks to discover identifiable biological differences between individuals with ADHD and without, and develop a definitive test for it, in order to steer clear of misdiagnoses and remove the stigma surrounding it. To achieve this, psychology has to merge with neurology. Neuroscience has revealed through various neuroimaging studies that ADHD patients do have differences in the brain compared to healthy controls, for instance, having smaller total cerebral volume, delayed brain maturation, and less white matter, a type of tissue in the brain that is responsible for the communication between brain regions. Some scientists have even developed machine learning approaches to distinguish ADHD patients from controls with data obtained through functional magnetic resonance imaging (fMRI), a neuroimaging technique. Unfortunately, those algorithms may not be able to diagnose ADHD on their own yet because ADHD cannot be attributed to the dysfunction of specific brain regions, but a multitude of brain anomalies and etiologies. Though, they are not without utility as they could be an objective and reliable screening method to assist clinical diagnoses by psychological methods by human professionals, mitigating variations among them.
03 The knowledge of neurological differences between ADHD patients and other individuals and novel methods of diagnosis clear up misconceptions and stigma surrounding ADHD. It is definitely helpful to relieve the stress placed on patients due to stigmatization, as the symptoms of ADHD already create great obstacles to patients and those around them. Not only do patients underperform in school during childhood and adolescence, ADHD is carried into adulthood for some, straining interpersonal relationships and butchering employability in the long run. Major long-term longitudinal studies estimated that 10 to 20% of patients with childhood ADHD develop antisocial problems later in life, such as having poor temper in social situations and committing crimes. The extra barrier of social discrimination is removed through establishing an objective understanding of the condition among the public, allowing patients to interact with others and achieve well-being more easily. This is an instance in which psychology and neurology combine as neuropsychology to enhance our understanding of the very nature of our minds, and attempts to improve the lives of many by sharing the knowledge. Yet even so, the essential part of making patients’ lives better is our own willingness to accept that knowledge, respect those who are different from us, and create a safe space for them. References https://www.cdc.gov/NCBDDD/adhd/data.html https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993524/ https://www.nhs.uk/conditions/attention-deficit-hyperactivity-disorderadhd/diagnosis/#:~:text=There's%20no%20simple%20test%20to,with%20you%20or %20your%20child https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4443828/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884954/ https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2019.19050540 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3016271/ https://adc.bmj.com/content/90/suppl_1/i2 https://www.fortunejournals.com/articles/longitudinal-studies-of-antisocialoutcome-in-individuals-with-childhood-attention-deficit-hyperactivitydisorder.html https://www.eurekalert.org/pub_releases/2020-12/uot-oif121520.php https://www.additudemag.com/overcoming-adhd-stigma/
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FUNCTIONAL NEUROIMAGING AND DEPRESSION By Tina Liu
Do you know that the activities of the neurons in our brain are constantly fluctuating as we engage in daily activities, no matter if the action is simple or not? Even on occasions when we close our eyes and rest, our brain remains highly active. To measure and map brain activities and improve understanding of certain brain areas, functional magnetic resonance imaging (fMRI) is often applied. Now, let’s find more about this technique. An overview of fMRI The fMRI technique was invented in 1990 by a group at Bell Laboratories led by Seiji Ogawa. It measures brain activity by detecting changes associated with blood flow. When a certain brain region is activated, it calls out for more oxygen. The fMRI will then follow oxygenated blood as it flows through the brain. On the printout of the scan, these oxygenated brain regions will appear to be lit up. The areas scientists can see are smaller than a millimetre cubed, or a voxel (a pixel in three dimensions). The major goal of fMRI data analysis is to detect correlations between brain activation and a task the subject performs during the scan.
05 Advantages of fMRI fMRI has several elementary features which contribute to its unmatched performance in neurological applications. First, fMRI does not involve any radiation such as X-rays during the process. If done correctly, fMRI has no risks and can evaluate brain function in a safe and non-invasive manner. It is easy to use, and can produce an image at a very high resolution, making fMRI very effective. Compared to other methods of psychological evaluation like questionnaires, fMRI is certainly more objective. Moreover, the clinical convenience provided by fMRI is worth noticing. As fMRI is performed with standard MRI scanners, the injection of contrast agents (responsible for stimuli) is avoided, as it can be achieved through the measurement of an endogenous contrast agent that is originally present at a high concentration in the brain. Lastly, fMRI enhances the possibility to study not only alterations in brain morphology that affect the activation of a certain region, but also its connectivity to other brain regions.
Clinical applications: How fMRI aid the diagnose depression Being the most common mental disorder in the world, depression had impacted around 300 million people. Common treatments for depression ranged from psychotherapies to counselling to taking medicines. For example, antidepressants compounded with psychotherapy will be recommended by doctors for patients having moderate to severe depression. However, although antidepressants are not generally dependency-forming, the misuse of such medicine can be dangerous. Hence, research shows that antidepressants may be more damaging than beneficial to health. As prescription drugs are a relatively new phenomenon to the human race, concern regarding whether chemical treatments interfere with the human brain also arises. Although depression is often treated as a single disease, many researchers tend to believe that it is a multiple ailment. While topics such as how depression subtypes and how they differ from each other are being debated over time, some try to correlate the neural circuits that light up during specific tasks with the patterns of activation with symptoms. fMRI is used in this process to provide doctors with a deeper look into the patient’s brain.
06 The RAD-AT STUDY An example will be The Research on Anxiety and Depression-Anhedonia Treatment (RAD-AT), a study led by Stanford clinical neuroscientist Leanne Williams, aiming at probing how depression manifests in the brain, hence discoveringhow it is associatedwith suicide. After years of studying, Williams has collected thousands of brain scans from people facing depression, hence discovering the existence of at least six subtypes of depression. Characterizing depression begins with the fMRI scanner, where the volunteers will lie while performing a list of mental tasks. Each task exercises a different assembly of circuits in their brains, corresponding to the six depression subtypes Williams has hypothesized. According to Brooke Staveland, a neuroimaging research engineer as well as a companion of Williams, the scan can reveal how different regions of the brain coordinate brain-wide neuronal chatter. However, despite the importance of fMRI in deciphering the pathogenesis of depression, the scan couldn’t capture symptoms that wax and wane as it is only a snapshot in time. As a result, fMRI was questioned by some neurologists for its effectiveness in reflecting the emotional fluctuation of the patient’s brain.
Social implications fMRI technique offers a powerful set of tools for observing experience-related changes. Researchers can look at the brain’s response to a particular input, such as a cognitive stimulus, a contextual setting or, in the clinical realm, a change in response to an intervention. Since the 1970s, some psychiatrists have encouraged the incorporation of fMRI into their field. With the advent of biological psychiatry, functional neuroimaging research on behavioural problems has exploded. Although functional neuroimaging has not yielded clinically relevant biomarkers for mental disorders, current studies lay the groundwork for its eventual use in the diagnosis, treatment, and prevention of behavioural problems and psychiatric disorders.
07 Critiques and challenges The technique of fMRI has always been facing complaints or challenges by many. One significant complaint is that fMRI only looks at the blood flow in the brain. fMRI measures blood flow and not neural activity directly because researchers assume that the blood flow correlates with neural activity. And although blood flow can reveal changes in brain areas as small as a millimetre cube, there can be hundreds of thousands of neurons in a tiny voxel. In this case, fMRI fails to hone in on neurons which are critical to mental functioning. On the other hand, as each area of the brain is made up of thousands of individual neurons and represent different functions, when a certain area is lit up on fMRI, it is hard to identify the exact type of brain activity being represented in the scan.
As most of the fMRI researchers are not trained in software engineering, they utilise one of several open-source analysis packages for pre-processing and statistical analyses. Hence, the attention to good software development practices that could help prevent errors is insufficient, and software errors may occur. An example of this would be shown in an article published in PubMed a few years ago, named AlphaSim: Software for Breeding Program Simulation. The analyses presented in a preprint of the present article contained two software errors that led to different results being presented in the final version of the paper. Because of these drawbacks, some critics even argue that fMRI is nothing more than a high-tech version of phrenology (the 19th-century pseudo-science that claimed to divulge a person's character based solely on the shape of his/her skull).
08 Solutions and how to pursue in the future Despite the critiques and challenges fMRI has faced, researchers still made suggestions to eliminate some of the problems, such as replacing custom code with software tools from well-established projects. By doing so, errors are more likely to be discovered when the code is used in a larger group and larger projects are more likely to follow better software development practices. Also, researchers should learn and implement good programming practices including the use of software testing and validation, to avoid such mistakes. In more recent years, a technique named “resting-state” fMRI (rs-fMRI) was developed. Here, research subjects are only scanned over a certain period without any involvement of active tasks. Rs-fMRI gave researchers a new and intriguing possibility for doing clinical fMRI, especially in cases where patients are severely affected like after a stroke or traumatic brain injury. Investigators are exploring novel applications of these techniques, hoping to increase the diagnostic sensitivity, accuracy and specificity, as well as the predictive value of the information.
Reference https://cfmriweb.ucsd.edu/Research/whatisfmri.html https://www.biorxiv.org/content/10.1101/059188v3.full.pdf https://www.sciencemag.org/news/2019/08/brain-scans-could-help-personalizetreatment-people-who-are-depressed-or-suicidal https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3787513/ https://www.ncbi.nlm.nih.gov/books/NBK538909/ https://www.nhs.uk/mental-health/conditions/clinical-depression/treatment/
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NEUROPSYCHOLOGICAL IMPLICATIONS OF INSOMNIA By Ivy Wong
As students, we are no strangers to late nights. Whether it’s homework, revision, nighttime socializing, or revenge bedtime procrastination, we frequently find ourselves staying up when we should most definitely be asleep. While we may keep ourselves up for various reasons, some people simply cannot fall asleep, however much they want to — insomniacs.
Insomnia: Persistent difficulty with sleep initiation, duration, consolidation or quality
According to the American Academy of Sleep Medicine’s ICSD-3 manual, “insomnia” is defined as “persistent difficulty with sleep initiation, duration, consolidation or quality.”, and is used to describe the presence of polysomnographic evidence of disturbed sleep. The condition’s prevalence in teens is as high as 23.8%, and as high as 60% among adults in some parts of the world. Insomnia is said to be caused by a state of hyperarousal, the disorder is frequently attributed to environmental, physiological, or psychological factors, such as stress, anxiety, consumption of certain substances, health problems such as sleep apnea, etc.
10 Effects of Insomnia on the Brain In a 2014 study published in the European Journal of Medicine, the R-fMRI results of 15 healthy patients were compared to that of 15 primary insomnia patients, connectivity was weaker between the superior parietal lobe (involved in attention and visuospatial perception) and dorsolateral prefrontal cortex (involved in executive functions including working memory and selective attention). Thus, one can conclude that insomnia leads to a decrease in task performance, backed up by a second study done in 2013 by UCSD. While there is no difference in objective cognitive performance between insomniacs and non-insomniacs, people with insomnia have trouble regulating activity in areas of their brain usually activated to perform the task. In the study, patients with insomnia showed increased activity in the dorsolateral prefrontal cortex, an area involved in working task memory. However, the brains of non-insomniacs showed no such increase in activity. Furthermore, a 2018 study shows that insomnia decreases gray matter around the dorsolateral prefrontal and middle cingulate cortices, as well as the frontal lobe. Gray matter contains most of the brain’s neurons’ cell bodies, and is heavily involved in decision making, emotion control, muscle control, etc. The frontal lobe controls important cognitive functions in humans, including but not limited to executive function, ability to communicate, problem solving, memory, etc. The reduction of gray matter around the frontal lobe implies a possibility of cognitive deficits in attention, executive function, and nonverbal memory.
While impaired function is commonly attributed to fatigue from the lack of sleep, it can be shown that insomniacs are affected cognitively on more than a psychological level. Thus, one can say that this leads to a more ‘socially acceptable’ reason for impaired functioning, as currently most are predisposed to accept a scientific reasoning over an emotional one.
11 Impacts: Affecting brain structure, insomnia also impacts daily functioning. The quality of life deteriorates due to the side effects of insomnia, such as fatigue, decreased ability to focus or communicate, decrease in mood, etc. This can lead to diminished functioning in day to day life, as well as affecting one socially, emotionally, and academically.
Insomniacs show subclinical levels of depression and anxiety, as well as a possible increase in suicide ideation, and insufficient sleep impacts one’s ability to regulate and evaluate emotion. Psychological explanations for the association between poor sleep and negative mood suggest a role for enhanced cortical arousal that leads to ruminations and difficulty sleeping. Neurobiological explanations, by contrast, suggest the dysregulation of the circadian pacemaker in the suprachiasmatic nucleus (SCN) in the hypothalamus, leading to neurobiological dysfunctions with a particular focus in the prefrontal cortex. As these regions (critical for modulating sleep processes, and for the regulation of mood and brain outputs from the amygdala) become unable to perform their roles, a plausible brain-system explanation for the link between poor sleep and negative mood is provided..
The hypothalamus plays a crucial role in our body, such as releasiung hormones and regulating body temperature
Apart from difficulties in mood, insomniacs frequently present with fatigue (which none of us are strangers to). For instance, 20% of car accidents happen with sleepiness as one of the main causes. Furthermore, their schedule is disturbed further as they try to make up for little or non-restorative sleep at night, by sleeping longer in the morning. While they may seem to be present, they are having microsleeps when awake, similar to a drowsy driver, they are less able to focus well, as well as more likely to respond slower to stimulus, and have a decreased ability to function. Their working memory capacity is also affected (as discussed above), and they have difficulty solving problems (e.g. mental arithmetic).
12 Further implications: Insomnia is often trivialised in relation to other comorbid conditions such as chronic pain, substance use disorder, cardiovascular disorders, etc. This is possibly due to the toxic culture rising up around work, in which workaholics are praised for neglecting their personal health in favor of their product. Sleep is seen as a ‘luxury’, as one can stay awake through willpower, caffeine, and various means. Thus, insomniacs are often seen as hardworking, or even envied for the ability to stay up later and complete more work. With the romanticisation of insomnia, the issue is trivialised, which is particularly concerning amongst teens and students who are still growing and thus need their sleep. However, as current society values work over personal health, competitive culture amongst colleagues or classmates often rises up around sleep (or lack thereof). However, taking into account its impact on cognitive function and emotional regulation, perhaps it should be taken higher into account. Abnormal cognitive profiles may be thought to be due to a psychological cause, when it is in fact caused by poor sleep. Alternatively, the impact of a co-morbid problem may be overestimated, and irregular performance may be attributed to poor motivation, poor effort, or anxiety issues. Sleep problems can also interfere with rehabilitation outcomes. The failure to resolve sleep issues will impact on rehabilitation, as interventions are less likely to be effective, as shown in Castriotta et al., 2009, in which insomnia impacts the degree to which cognitive rehabilitation helps patients who suffered traumatic head injuries. Sleep problems are also at a risk of causing complications if they remain undiagnosed. Clear links have been shown between sleep problems and increased morbidity and mortality (e.g. increased risk of heart conditions or diabetes). They also have a detrimental effect on neurological disorders by increasing the risk of stroke occurrence and outcomes. Finally, poor sleep degrades the quality of life of vulnerable populations and may hasten progression of neurological and psychological disorders. The higher prevalence of insomnia in women begins in adolescence, and it is especially high during menopause. Insomnia also has a higher prevalence in the elderly population and individuals with low socioeconomic status or poor baseline health. Furthermore, social or societal stressors are associated with insomnia. For example, studies show that the incidence of insomnia in homeless people was twice that of the general population (41% vs 19%). Insomnia is also well documented in patients of mental illnesses, such as depression, anxiety, PTSD, etc. In childhood disorders (such as ADHD), the lack of diagnosed sleep problems (as many as 1 in 4 remain undiagnosed) may heavily affect the development and severity of their disorders.
13 Coupling the debilitating effects of insomnia with the stressors and effects present in the lives of vulnerable populations, it can be seen that insomnia can greatly affect the quality of life of vulnerable individuals, piling on the side effects of insomnia on top of their already great suffering. Treatments: While your first instinct might be to turn to sleeping pills, studies have shown that sleeping pill users have a high risk of developing dependence and addiction to the medication. Furthermore, it has been postulated that sleeping pills (such as Xanax) are linked to higher chances of developing dementia. Instead, cognitive behaviour therapy has been suggested as a way of treatment for insomnia (CBT-I). Psychologists employ techniques such as stimulus control therapy (set a consistent time and place for sleep), relaxation training and meditation, remaining passively awake (avoiding any effort to fall asleep, letting go of the worry, and thus relaxing and making it easier to fall asleep), etc. A 2015 review of over 20 different CBT-I trials found that on average, insomniacs who used CBT-I fell asleep faster by 20 minutes and spent 30 fewer minutes awake. The reason why CBT-I is preferred over sleeping pills and other remedies is that it gets to the heart of the issues – the problematic attitudes and behaviors the patient has around sleep. By addressing the underlying reasons of insomnia, CBT can solve the problem at its root. While insomnia is common and tragically unavoidable for many of us, none of us, not even science, can deny the importance of sleep for day-to-day existence and functioning. So, if you’re lucky enough to not have insomnia, go to sleep!
14 Bibliography https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1978319/ Insomnia: Definition, Prevalence, Etiology, and Consequences, Thomas Roth, 2007 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6164454/ Insomnia in Adolescence., Innessa Donskoy and Darius Loghmanee, 2013 https://pubmed.ncbi.nlm.nih.gov/21249453/ Bastien, C. H. (2011). Insomnia: Neurophysiological and NeuropsychologicalApproaches. Neuropsychology Review, 21(1), 22–40. doi:10.1007/s11065-011-9160-3 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5860517/ The Effect of Insomnia on Neuropsychological Functioning in Patients with Comorbid Symptoms of Pain, Fatigue, and Mood Disorders https://www.researchgate.net/publication/51110003_Neuropsychological_Effects_ of_Sleep_Loss_Implication_for_Neuropsychologists https://www.brainforestcenters.com/news/how-chronic-insomnia-affects-thebrain https://link.springer.com/article/10.1186/2047-783X-19-32 Functional connectivity changes between parietal and prefrontal cortices in primary insomnia patients: evidence from resting-state fMRI https://pubmed.ncbi.nlm.nih.gov/29411240/ Li, M., Yan, J., Li, S., Wang, T., Wen, H., Yin, Y., … Jiang, G. (2018). Altered gray matter volume in primary insomnia patients: a DARTEL-VBM study. Brain Imaging and Behavior. doi:10.1007/s11682-018-9844-x https://www.mayoclinic.org/diseases-conditions/insomnia/in-depth/insomniatreatment/art-20046677 https://corpus.ulaval.ca/jspui/bitstream/20.500.11794/33346/1/Art_2012_Sleep%20 Med%20Rev_Fortier_Brochu_Insomnia%20and%20daytime%20cognitive%20perf ormance%20A%20meta-analysis.pdf https://www.ajmc.com/view/insomnia-overview-epidemiology-pathophysiologydiagnosis-and-monitoring-and-nonpharmacologic-therapy
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TIME PERCEPTION By Heather Lo
Do you ever feel that time could not pass by anymore slower when you are almost late for school but are still waiting for 12A at Admiralty bus-stop? However, time feels like rushing past when we are on holiday and are having fun? To explain this, let us learn more about time perception. Definition and overview Time perception is a fascinating and interesting phenomenon. It is one of the most important topics of neuropsychology (a branch of psychology that studies human behaviours with neurological observations). It is defined as how our brain estimates time intervals and duration. By studying how patients with dorsolateral prefrontal right cortex lesions perceive time differently from those with intact right cortex, neuroscientists believe that the dorsolateral prefrontal right cortex is the region most involved in time perception. Time perception can be explained from the neuropsychological, cognitive psychological, philosophical and other perspectives. In this article, we will focus on the neuropsychological foundation of time perception. Every one of us has an internal clock. Time perception can be accurate, but sometimes it can be inaccurate. The inaccuracy of our time perception is not the result of a malfunctioning internal clock. In fact, the perception of time is a complex neural mechanism that can be influenced by our emotional state, level of attention, memory and diseases. It shows our ability to adapt to events happening around us. Time flies more quickly when we are busy or having something fun. However, minutes drag by when we are bored, worried, anxious or frustrated.
16 Theoretical explanation of time perception Neuropsychologists believe humans have a system to govern time perception. They proposed different theories to explain the mechanism of time perception. The most well-known model, which is also the earliest one to explain time perception, is called the scalar expectancy theory. This theory can be explained by the pacemaker-switch-accumulator mechanism. It suggests that our brain perceives time as a synchronized ticking of our internal clock. The closing action of the switch in the pacemaker is controlled by our attention. When the stimulus is focused, the impulses flow to the accumulator. The switch then reopens, interrupting the flow of the impulses. Therefore, the time intervals are calculated. When the time interval speeds up, it makes us feel that time is passing slowly. When we stop paying attention to time, the beats are not counted. As a result, it appears that the duration is shorter than in reality (that is, time is passing quickly). In 2005, Professor Warren H. Meck proposed a physiological model to explain time perception. It suggests that the vibrating activities of brain cells in the upper cortex support time perceived by our brain. The vibration of each cell creates a beat. Cells in the dorsal striatum, at the base of the forehead, then detect the frequency of vibration. Hence, the time is estimated.
Our brain perceives time as a synchronized ticking of our internal clock
17 Chess Stetson, Matthew P. Fiesta, and David M. Eagleman conducted a study on “time-slowing” during frightening events. In their study, participants were asked to experience free fall. They were asked to estimate the time between the beginning of the fall and landing on the ground. The results find that participants estimated the duration of their own free falls 36% longer than the others’. The results suggest that our brain estimates duration based on the amount of data and memory we store. The more data our brain receives within the period of time, we perceive that the duration is much longer than its actual duration. When participants experience the fall on their own, their brains accumulate a tremendous amount of memory in an unusually short period of time. Therefore, they estimate that the duration of the falls is a much longer duration. On the other way round, if our brain receives very little data, we feel that time passes very quickly. When participants were asked to watch others’ free falls and estimate the duration of their falls. In other words, these participants did not have the first-hand experience of the fall. The duration they estimated was shorter than that estimated by those who did the free fall. Conclusion This article discussed the neuropsychological foundation of time perception. Time perception changes with our emotional state, level of attention, memory and diseases. It can be used to explain various time-related daily experiences and observations.
References https://hbr.org/2016/05/different-cultures-see-deadlinesdifferently#:~:text=Western%20cultures%20tend%20to%20view,operations%2C%20 by%20milestones%20and%20deadlines.&text=Other%20cultures%20perceive%20ti me%20as%20cyclical%20and%20endless. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4142010/ https://www.theguardian.com/science/2013/jan/01/psychology-time-perceptionawareness-research https://link.springer.com/content/pdf/10.3758/BF03194099.pdf https://storage.googleapis.com/plos-corpusprod/10.1371/journal.pone.0001295/1/pone.0001295.pdf?X-GoogAlgorithm=GOOG4-RSA-SHA256&X-Goog-Credential=wombat-sa%40plosprod.iam.gserviceaccount.com%2F20210330%2Fauto%2Fstorage%2Fgoog4_request &X-Goog-Date=20210330T162659Z&X-Goog-Expires=3600&X-GoogSignedHeaders=host&X-GoogSignature=30204db7e3185882cc7368db795f246d53a
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NEUROPSYCHOLOGICAL FUNCTIONING IN BIPOLAR DISORDER By Christine Pang
Introduction to Bipolar Disorder (BD) – diagnostics, symptoms & identification: Bipolar disorder is one of the most distinguishable mental illnesses in the course of history because of its apparent symptoms – extreme shifts in the mood, activity levels, and energy of bipolar patients. It is also known as the manic depressive disorder because of the emotional “highs” and “lows” experienced by its patients. During a hypomanic or manic episode (mania), bipolar patients have the following characteristics and symptoms: feeling elated, adventurous, and confident; sleeping very little, approximately 2-3 hours a day; yet being able to maintain a high energy level, feeling extremely restless and impulsive, talking a lot, and speaking very quickly with racing thoughts. On the contrary, during a depressive episode, bipolar patients have almost completely opposite behaviours: feeling upset, worthless, or hopeless; sleeping too much to the extent that it disrupts their daily functioning; isolating themselves from social interactions, or even attempting suicide.
19 Neuropsychology and Bipolar Disorder:
So how can we explain the above traits of BD in a more scientific manner? What can we extrapolate from the neuropsychological perspective of BD? In fact, various neuropsychological studies have been carried out to examine the impairments in executive functioning, decision making, and goal achieving in both hypomanic and depressed bipolar patients to elucidate their state-and-trait-related changes. In order to understand the neuropsychological functioning in bipolar patients, we first have to know the functional contributions of two brain components - the amygdala and ventromedial prefrontal cortex (PFC). The amygdala is critical for both punishment and reward based reinforcement associations, in which positive reinforcers add positive stimulus, and negative reinforcers remove aversive stimulus in order to maintain our “normal” behaviours. It also contributes to the processing of emotional expressions. PFC is critical for the representation of reinforcement expectancies and decision making. Within the brain, the amygdala is the reaction centre that responds to threats, and the PFC is the reward centre. The amygdala develops earlier than the PFC and is associated with quick emotional responses. In the hypomanic or manic phase of bipolar patients, it appears that the amygdala in the patient’s brain is not sending appropriate signals and is providing misinformation to the PFC. The hypersensitivity of amygdala and the PFC give rise to risk-taking and reward-seeking behaviours, which manifest as impaired judgments, reckless actions, and dysregulation in goal pursuits. This cognitive dysfunction explains the talkative, confident, yet thoughtless or irrational characteristics of bipolar patients during their hypomanic or manic episodes. On the other hand, in the depressive phase of bipolar patients, the abnormally elevated activity of the amygdala in the left prefrontal cortex of bipolar patients tends to inhibit serotonin. According to the serotonin hypothesis in depression, low levels of the neurotransmitters serotonin arouse sad, fearful, or agitated emotions which contribute to the depressive episodes of bipolar patients. Hence, the negative emotions engendered by serotonin inhibition causes disruption of daily functioning and withdrawal symptoms in depressive bipolar patients, such as hypersomnia (over-sleeping) and self-isolation in interpersonal relationships.
20 Social implications of bipolar disorder, misdiagnosis and solutions: The critical functions of the amygdala and PFC as mentioned above are compromised in individuals with the disorder. Neuropsychological impairments and cognitive dysfunctions in bipolar patients can significantly contribute to social and occupational difficulties, reduced insight, increased risk of non-adherence (meaning that the patient actively decides not to use treatment or follow treatment recommendations) and a higher chance of relapse.
Bipolar disorder may often be misdiagnosed as “unipolar” depression because they both are associated with similar cognitive and neuropsychological deficits. To the present day, neuropsychologists still have not come to an agreement on the distinctive cognitive profiles of bipolar disorder and unipolar depression. Although studies have been carried out to compare the neuropsychological functioning in bipolar disorder and major depressive disorder, the evidence obtained could not be used to elucidate the differences between the two disorders due to the uncontrolled variables (like age, medication status, bipolar subtype etc.) which may affect the cognition of patients involved in the studies. Other than unipolar depression, bipolar disorder may also be misdiagnosed as attentiondeficit hyperactivity disorder (ADHD). When bipolar patients are in their manic phase, they tend to manifest symptoms that are very alike to ADHD, such as hyperactivity, impulsivity, attention and memory impairments. Both disorders have similar cognitive profiles which, likewise with bipolar disorder and depression, do not allow psychologists to clearly differentiate bipolar disorder and ADHD. The consequences of misdiagnosis of bipolar disorder are profound and destructive to patients as they would not be able to receive effective treatments to cure their mental illnesses. This may give rise to a greater number of recurrences and complications or more long-term episodes, both manic and depressive.
21 Despite the hurdles and difficulties faced by bipolar patients, evidence has shown that bipolar symptoms can be treated with certain psychiatric medications, which are known to act on the neurotransmitters (messenger chemicals) in the patients’ brains. In the short term, medication can be offered to both manic or depressive bipolar patients to stabilize their physiological and mental states. In the long term, offering cognitive behavioural therapy to bipolar patients can help them to clear their emotional and social recovery goals. Coming up with a crisis plan can also help bipolar patients and their family members to know what to do when the patient shows any sort of early warning signs, symptoms or distress.
As with all mental disorders, communication is key!
References: https://www.mind.org.hk/mental-health-a-to-z/bipolar-disorder/about-bipolardisorder/ https://progress.im/en/content/how-does-brain-change-bipolar-disorder https://www.ajmc.com/view/oct05-2151ps271 https://www.sciencedirect.com/science/article/abs/pii/S016517811630782X
