prefrontal cortex

Consciousness – Who decides, 𝘺𝘰𝘶 or your brain?

Posted on by Iasmina Hornoiu

If you were to answer the question “What differentiates humans from other organisms on Earth?”, you would probably list a number of things, including the ability of humans to make “free choices” dictated by their consciousness, rather than by something organic. Am I right?

What if someone told you that this is not actually the case? I mean, what if instead of making decisions out of your own will, your brain is “deciding” for you and only after the decision has been made the brain offers you the illusion of conscious act, making you believe that you were the one who made the choice in the first place. But how is it possible that such a dichotomy exists within ourselves, between us and our own brains? Aren’t we our brains? Apparently not!

Now that I (hopefully) managed to capture your attention, I’d like to bore you a bit with some brain structure names and functions, which are necessary in order to begin to understand what’s going to come next.

The frontal lobe contains a few areas, which are involved in planning our movements, decision-making, emotions (usually associated with the decisions we are about to make), repeating previously memorised motor sequences etc. These are the areas involved in voluntary motor control, more specifically, these are the areas that make the difference between reflexes/automatisms and movements or actions we want to pursue. Moreover, all these motor areas are interconnected and also linked to areas that are part of the sensory pathways, such as the parietal , visual, somatosensory and temporal regions (which store different components of visual, auditory and somatic stimuli and are associated with many diseases, such as the inability to feel your own limbs, or recognising faces/objects etc.).

  • The primary motor cortex (PMC) is mainly involved with the execution of movements. Populations of neurones in there encode for the direction and amplitude of the movements we make, prior and during the execution.
  • The 6 pre-motor cortices, the ventral, medial (supplementary) and dorsal areas are mostly involved with planning our movements. They receive inputs from the cerebellum and basal ganglia, which play very important roles in motor learning (like acquiring new skills) and motor planning. Interestingly, different neurones in the pre-motor areas fire action potentials during execution and are inactive during planning of movements and others vice-versa, while some populations of neurones are active for both planning and execution.
  • The prefrontal cortex controls reasoning and decision-making and it is crucial for emotion as well: recall Phineas Gage’s story and how the damage to his prefrontal cortex resulted in a complete change in his personality (article here) as well as how the prefrontal cortex regulates the activity in the hypothalamus and is disrupted in major depressive disorder (article here). 
  • The limbic system (amygdala, anterior cingulate cortex, hippocampus) , which are located at the subcortical level and behind the frontal lobe, are involved with emotion, fear and the formation of memories, which are so important in our decision making. And these are just the main players, but there are many other areas, including sensory, which contribute to the planning of our actions and the choices we constantly make.

In a rather groundbreaking paper, Libet and colleagues showed that the neural processes leading to the initiation of voluntary movements begin several hundred milliseconds before the reported time of conscious intention to make the movements, as in before the subject is aware of the intention to move. They demonstrated using the readiness-potential (negative electrical potential recorded at the scalp) that brain activity involved in decision-making starts before our brains is conscious of the actions. This is also known as ‘preparatory set”.

Dick Swaab proposed that the unconscious brain areas are active before the conscious ones, in order to enable us to make decisions rapidly and effectively, as the conscious systems require time to process and analyse the pros and cons of every decision. And although it is good to consider the consequences of your actions, there are many other decisions about apparently insignificant things, which we make and need to be fast (like for example, running away from a car you see coming). In a dangerous situation, for example, the parts of the brain involved in consciousness might consider the state of your legs, how capable they are of moving fast at that point, your heart rate, blood pressure, levels of energy needed for that action…Well, by the time your brain finishes analysing all these, you will be most certainly dead.

Another interesting idea Swaab suggested was regarding the reason why we have consciousness of our actions and the things that happen to us in the first place. We need to be conscious of our own experiences so that we learn to avoid negative things in the future and also act upon things that require intervention, such as a wound that needs to be treated. Although the brain seems to be able to plan an action independently of our awareness of it, other brain areas are involved in the execution (as previously mentioned) and the communication between these different parts which fulfil different roles results in consciousness. Exactly why and how evolutionary biology has managed to make us more than just some purely mechanical creatures remains a mystery and still poses many challenges to this field of research, inviting philosophy to have its take on this matter, which many times has proved to be useful.

Swaab also wonders to what extent are criminals, pedophiles, murderers to blame for their bad actions, when it is in fact not them, but their unconsciousness/instincts that dictate them what to do. When considering that people with brain damage resulting in impaired or lack of consciousness (schizophrenia, dementia, multiple sclerosis etc.) sometimes hurt other and are not convicted, you might think that it is right to assume that all criminal acts should be tolerated. However, the difference here is that people not suffering from such disorders are aware of their actions and are capable of stopping them. Although pedophilia is considered a psychiatric disorder, unlike the neurodevelopmental and neurodegenerative ones, it can be controlled by the individual, so that the individual is able to refrain from acting according to his/her instincts. Libet and his team of researchers mention in their study that individuals, although only aware of the intention to make a particular action after the intention has been formed in their brains, are able to “abort the performance” of the action, meaning that they have a conscious “veto”.

They also emphasise the difference between spontaneous, rapidly performed actions, and actions in which a preplanning of the experience occurred (taking into account alternative choices, for instance). This second type of voluntary movements, involving conscious deliberation prior to the act, might actually rely on conscious initiation and control, rather than non-conscious commands. However, this hypothesis has not yet been proved experimentally, in a way the “unconsciousness before consciousness” one has.

So, as it turns out, most of the times we are aware of our brain’s decisions only after they have already been made, and free will seems to be an illusion.

References

Libet et al. paper

Antonio Damasio,1995. Decartes’ Error. Vintage Books, pp. 71-73

Dick Swaab, 2014. We are our brains – From the womb to Alzheimer’s. Penguin Books, pp.326-338

Image by Saya Lohovska. You can find her arts page here.

Depression and why some of us are SAD

Posted on by Iasmina Hornoiu

I am warning you, this is going to be a long one! But it’s interesting, I promise.

There is a lot of confusion and mixed opinions when it comes to depression. Some people use the term inappropriately, to describe what is in fact grief (the feeling of sadness that humans, and presumably other animals, experience after a loved one has died, for instance), others tend to label depressed individuals as “weak”, “selfish”, “useless”, “cowards” etc.

At the same time, for the past 30 years, there have been extremely important discoveries in the field of affective disorders, which have helped eliminate many misconceptions and laid the foundation for a better understanding of what this set of disorders (affective disorders) are and what is actually happening in the brain of the ones “affected”. Moreover, according to some new theories, depression is in fact an evolutionary advantage in situations such as physical illness and dominance. When the body is sick it needs time and energy in order to recover, so the organism experiences depression in order to avoid activity and focus on recovery; in nature, many animals with a dominant status are forced (by a variety of factors) to occupy a lower hierarchical level, in which case “depressive” behaviours such as avoiding eye contact or sexual contact helps reduce the risk of attack by other dominant, more powerful individuals. There are many theories, as you can see, and this article is meant to present and analyse some of them.

We should start by clarifying a very important aspect: depression is different from grief. While the latter is a normal reaction to some external factor(s) with a negative emotional impact on our day-to-day lives, and dissipates by itself after a certain period of time, depression is a pathological, abnormal condition (either in its own right or as a symptom of other metabolic or neurodegenerative diseases). However, it should be noted, and this is one of the key concepts in understanding depression, that the way individuals interpret and react to various external events, which affect their mood, differs, which means that some individuals have a stringer predisposition to depression than others. Now, why is that? A variety of factors, both genetic and epigenetic (developmental, such as child abuse, neglect) play a role and often act synergistically, but we will deal with them (especially, the genetic factors) a bit later in the article.

Different types of depression

Major depressive disorder, also known as “the classical depression”, which is characterised by insomnia, anorexia and lack of joy and interest in things. At the opposite side of the spectrum, there is atypical depression, which manifests itself through increased sleepiness, weight gain and anxiety. Dysthymia is another form of depression, more difficult to diagnose, due to the fact that it presents itself with mild depressive symptoms. All these types discussed so far have been categorised as monopolar.

Bipolar depression refers to a kind of depression accompanied by periods of mania – manic episodes are characterised by elevated, euphoric mood, impulsiveness, hyperactivity and even psychotic symptoms (hallucinations, delusions). A case described by Dick Swaab in his book “We are our brains – from the womb to Alzheimer’s” portrays a woman, who developed mania following the death of her husband. She would talk and laugh hysterically, call the police in the middle of the night for no reason and eventually began to make up stories about people whom she had never met before, but who she believed were longtime friends of hers. After her manic episodes disappeared as a result of treatment, she developed severe depression. Luckily, her story has a happy ending, as she made a full recovery.

Bipolar depression is also associated with Seasonal Affective Disorder (SAD), characterised by extreme mood seasonal swings. In this article, I have dedicated an entire section to SAD, so I am not going to delve into it for now. Given all these particularities of BD, it is often regarded as a separate disorder (bipolar disorder or manic disorder), rather than another type of depression. As there are so many things to mention about depression, I will leave BD for future article.

Diagnosing depression

In order to be diagnosed with depression, one must have at least one of the two main symptoms: persistent sadness and marked loss of interest, as well as at least five secondary symptoms: disturbed sleep (either increased or decreased), disturbed appetite (increased or decreased), fatigue, poor concentration, feeling of worthlessness and excessive guilt, suicidal thoughts.

Depending on the number of these symptoms, as well as the degree to which they manifest, monopolar depression can be sub-divided into: sub-threshold depression (fewer than five secondary symptoms; no treatment needed), mild depression (fewer than five, but in excess secondary symptoms), moderate depression (more than five, plus functional impairment between mild and severe depression) and severe depression (most of the secondary symptoms and also true psychotic symptoms – yes! they can occur in severe monopolar depression as well, not just BD).

Biochemical pathways and brain systems involved in depression

In Ancient Greece, there was a biochemical theory of depression. It was believed that depression was caused by the failure of liver to eliminate toxic substances from the digested food, resulting in the accumulation of “black bile” (melan means “black” and chole means “bile”, which give the words melancholy). Biochemical theories nowadays have at their core three monoamines, which I am sure you are all familiar with: noradrenaline (a neuromodulator very similar to adrenaline) and serotonin and dopamine.

These two substances have long and diffuse projections throughout the nervous system and in levels lower than otherwise normal, they are said to be involved in affective disorders. For example, drugs such as Reserpine, used to treat the positive symptoms of schizophrenia by depleting dopamine (and also serotonin and noradrenaline) elicited depressive symptoms in schizophrenic patients.

Therapies involving monoamines

The idea is, you want to higher levels of monoamines in order to treat depression. Enzymes involved in the monoamine re-uptake mechanism from the synaptic cleft back into the presynaptic level and enzymes involved in the monoamine metabolism, such as monoamine oxidases (MAO) are the most common targets for the majority of anti-depressants.

  • Selective serotonin re-uptake inhibitors (SSRI) and selective noradrenaline re-uptake inhibitors (SNRI) – Prozac (Fluoxetine), Zoloft (Sertraline), Celexa (Citalopram), Paxil (Paroxetine) block serotonin reuptake and Effexor/Viepax/Trevilor/Lanvexin (Venlafaxine), Cymbalta (Duloxetine) inhibit the noradrenaline reuptake enzymes. For those of you who are currently under this treatment, be careful! Side-effects such as sexual dysfunction, insomnia, increased aggression and self-harm/suicide can occur. Moreover, SSRI are not so effective. They have a very long induction, which means that it takes a long time (2-3 weeks) for the therapeutic effects to start working, during which time there is a high risk of suicide (due to depression). They also have a placebo effect of 50%, which is not necessarily a bad thing as long as it works, but raises the question whether the monoamine hypotheses is really that valid in the case of depression.
  • Tricyclic antidepressants – also block the reuptake mechanism, resulting in more monoamines in the synaptic cleft. Amitril (Amitriptyline), Aventyl/Norpress/Noritren (Nortriptyline) and Tofranil (Imipramine) are a few examples. They are derived from Phenothiazines (such as Chlorpromazine), which are antipsychotic drugs (used to treat schizophrenia). Some of the side-effects are: chronic pain and suicide overdose.
  • MAO inhibitors – Nardil/Nardelzin (Phenelzine), USAN (Thanylcypromine), Marplan/Enerzer (Izocarboxazid) and Amira/Aurorix/Clobemix (Moclobemide) are very effective and widely prescribed for in major depressive disorder, bipolar disorder and anxiety disorder, although the first three pose the high risk of hypertensive crisis and death if the patient is consuming cheese or wine.

The big problem with these drug therapies is dependence – if antidepressants, especially Paroxetine and Venlafaxine are administered for a long period of time and then stopped, the patient is likely to experience Antidepressant discontinuation syndrome, characterised by flu-like symptoms, motor and cognitive disturbances.

Non-drug therapies

An alternative to pharmaceutical treatments is represented by transcranial magnetic stimulation (TSM) of the cortex, electroshock therapy – this is, apparently, very effective, BUT might result in impaired memory – and gene therapies. The latter refers to the insertion, via a vector or a plasmid, of genes that encode neurotransmitter molecules, receptor proteins or neurotrophic and neuroprotective substances. Given that many variations in genes for chemical messengers in the brain are responsible for the predisposition of certain individuals to depression, gene therapies, although still at a developing stage, provide powerful approaches to the treatment of affective disorders.

Over-activation of the stress axis

Another theory for the development of depression, which goes hand-in-hand with the “monoamine hypothesis” is that in depressed individuals there is an exaggerate amount of cortisol (a steroid) in the blood, which can affect the brain. Basically, our brains react to stressful situations by producing some hormones in the hypothalamus and pituitary gland (hypophysis), which eventually result in the production of cortisol. In turn, cortisol acts on these structures to inhibits their activity and, thus, preventing further increases in its level – this is an example of a negative feedback mechanism.

In normal people, a stressful situation will result in increased levels of cortisol, but this steroid will then revert to its normal levels. In depressed individuals, the stress axis (hypothalamus-pituitary-adrenal axis) becomes hyperactive and, as a result, a stressful event will result in the overproduction of cortisol.

In excess, cortisol affects brain structures involved in the control of emotions and fear, such as the cingulate cortex and amygdala (which explains the anxiety symptoms experienced by people suffering from atypical depression) and memory, such as the hippocampus, which explains the cognitive dysfunctions. Moreover, the activity in the prefrontal cortex, which normally inhibits the hypothalamus (overactive in depression) is decreased by cortisol. So, really, it is like a vicious circle.

Why is the stress axis hyperactive in the first place? Possibly due to decreased sensitivity of the cortisol receptors to cortisol, which might be the result of genetic as well as developmental factors (previously mentioned).

Monoamines play a role here, as increased levels of monoamines (by the administration of antidepressants) can determine neurogenesis in the prefrontal cortex and hippocampus, so these areas can function properly again and can, thus, inhibit the hypothalamus, so no longer hyperactivity of the stress axis!

Seasonal affective disorder (SAD)

Although I am planning to write about bipolar disorders in another article, I thought it is worth discussing SAD in this article as well, given that so many people, especially those living in the Northern hemisphere, suffer from it.

In the References section there is a document called “The recent history of seasonal affective disorder (SAD)”, which is a transcript of the 2013 Witness Seminar in London. I highly recommend this reading for two reasons: it is full of remarkable, extremely important information regarding SAD and the participants at this seminar included personalities such as Prof. Josephine Arendt, Prof, Norman Rosenthal, Prof. Alfred Lewy, Prof. Rob Lucas, who are pioneers of the SAD diagnostic criteria and underlying causes (for instance, Rosenthal is the first psychiatrist who diagnosed SAD).

As many of you probably know, and sadly from personal experience, SAD is a seasonal mood change disorder, a type of bipolar disorder, which determines depression during the autumn/winter seasons and hypomania during summer. In order to understand SAD, we must remember a few things about the circadian rhythm, which I have previously discussed in two articles: Why “sleep” and Even flies sleep and learn. In short, we have an internal, genetic “clock” inside our brains (in the Suprachiasmatic nucleus – SCN), which determines the body to function in an approximately 24-hour cycle and which is also entrained by the light-dark cycle. This is not only a circadian (day-night) clock, but also a seasonal clock, which means that changes in the environment (especially light and temperature) across the year entrain this clock and determine physiological and psychological changes in our bodies.

In SAD, there is an abnormal secretion of melatonin (the hormone that triggers sleep, when it is dark outside). Light inhibits this hormone: cells in our retina, which are not coding for visual information, send projections via a distinct pathway than the rods and cones. These cells, containing  the peptide melanOPSIN, project via the retinohypothalamic tract to the SCN, “telling” the brain that it is dark outside, so the brain (SCN) determines the synthesis and release of melatonin from the pineal gland. When there is light outside, the production of melatonin is inhibited. The duration of melatonin secretion is also affected by the circannual changes – long secretion in short days and short in long days. The scientists who took part in the Witness Seminar discovered that melatonine production was increased during the depressive/winter phase and that sunlight decreased its production, thus, alleviating the symptoms of depression in SAD. A note here, sunlight is an effective treatment for SAD, not ordinary room light. This explains why, during winter, when people tend to spend more time indoors, their levels of melatonin increase. The reasons why room light does not inhibit melatonin production are the intensity of light (sunlight is five times more intense than room light) and spectral differences. More about SAD and bipolar disorder in a future article!

I hope this article made sense and that you enjoyed reading it!

References
SAD – Pdf of The Witness Seminar transcript

Beatty, 2000. The Human Brain – Essentials of Behavioural Neuroscience. Sage Publications. Inc., pg.464-471

Dick Swaab, 2014. We are our brains – From the womb to Alzheimer’s. Penguin Books, pp. 112-122

Image by Damaris Pop

Why “sleep”?

Posted on by Iasmina Hornoiu

In a previous article, we talked a bit about narcolepsy as one of the very intriguing sleep disorders. It was perhaps easy to understand why people suffering from narcolepsy could have a pretty hard time performing several normal tasks; however, most of us would probably relate less to narcolepsy. But something which almost everyone can agree to have experienced regularly, in one way or another, is sleep. In comparison with disorders associated with it or derived from its impairments, sleep itself might not seem so interesting. We all do it and we can’t deny how much we enjoy it and long for it after it stops. Yet, there is much more to sleep than we think.

Sleep is very important for the normal functioning of any being. For animals as well as for humans, sleep helps in energy conservation, body restoration, predator avoidance and learning aid. Different animals have different sleep-wake cycles, from nocturnal animals (like rodents), which sleep during the day and are active at night, and animals which sleep with only half of the brain (like dolphins), all the way to diurnal animals, like humans. Although humans are advised to sleep approximately 8 hours per night, some people sleep very little (around 2-3 hours/night) and still function perfectly fine. An example of such a situation is presented in the textbook of Rosenzweig et al. (pg. 389).

But what triggers sleep and how is it regulated?

Most of us are certainly able to recall a dream the next morning and the memory of that dream is usually accompanied by feelings and emotions we sometimes do not even experience in real life. We are often under the impression that our dream has lasted the whole night. In fact, there are two stages of sleep, one of which is associated with the formation of dreams. These stages, known as non-REM sleep and REM sleep, succeed each other in cycles lasting approximately 90 minutes. Just to define the terms, REM means rapid eye movement and represents the part of sleep with the most increased brain activity. Interestingly, during REM the brain seems to consume more oxygen than during arousal!

Normally, when we fall asleep we slip into the non-REM stage or the slow-wave sleep (SWL). This, in turn, is divided into four other stages: from light sleep to very deep sleep. During this phase, the brain is said to be truly resting and the body appears to repair its tissues. No dreams can be seen! The movement of the body is reduced, but not because the muscles are incapable of moving; it’s the brain which does not send signals to the body to move! One interesting feature of non-REM sleep is sleep-walking. This peculiar behaviour some people show while asleep usually takes place during the fourth (last) part of the non-REM sleep, when the person is the deepest sleep. This is the reason why it is very difficult to wake a sleepwalker up.

In turn, REM sleep (which starts after a 30-minute non-REM period) is the “active” part of our sleep. This time, the brain sends commands to the body, but the body seems to be in an almost complete state of atonia (immobility). The heart rate and breathing become irregular and the brain is not resting. In fact, our dreams happen during this time and more importantly, our long-lasting memories are thought to be integrated and consolidated.

FullSizeRender-2

When it comes to sleep regulation, many neuroendocrine systems and brain functions play a role. The circadian (or sleep-wake cycle), which is controlled primarily by the suprachiasmatic nuclei, in the hypothalamus, need special attention. For the purpose of this article, I won’t focus on the circadian clock now, but I will come back to this in a future article. The autonomic nervous system and parts of the brain such as the brainstem, the limbic system, especially the amygdala, and the forebrain modulate different aspects and stages of sleep. Amygdala, which I mentioned in a previous article about emotions and decision-making, is a brain region involved in the emotions such as fear. It also appears to be very active during REM-sleep and may account for the awful nightmares we often experience.

Many cognitive functions, such as intelligence, performance and emotions are associated with disrupted non-REM as well as REM sleep. To be more specific, REM-sleep loss appears to be associated with increased anxiety and stress and loss of emotional neutrality – this means that a person deprived of REM-sleep is more likely to react negatively to neutral emotional stimuli than in normal conditions. The explanations vary, but most of the studies agree that impaired REM sleep triggers increased release of noradrenaline, hyperactivity of amygdala and decreased function of prefrontal cortex (which tells “stop!” to the amygdala when it goes crazy). At the same time, people deprived of non-REM sleep could experience depression, due to deficiency in another neurotransmitter, this time an inhibitory one, called GABA (gamma-aminobutyric acid). Other problems linked to sleep deprivation are attention deficits, working memory impairments and usually affected divergent thinking (creative, innovative thinking).

Aging people seem to sleep less and this deprivation is also associated with conditions like Alzheimer’s. Moreover, sleep deprivation can kill you! Sustained sleep loss can cause low immune system and drop in body’s temperature, which can make bacterial infections fatal. Another consequence of sleep loss is increased metabolic rate, which leads to weight loss and eventually death. Don’t think this could be a good idea for a diet! More like for “die”!!! Having said that, most people should try their best to get enough hours of sleep.

I hope this article convinced you of the importance of sleep and as usual, any questions or comments are welcome 🙂

Further information:

Article 1 – about REM-sleep and emotional discrimination 

Article 2 – about non-REM sleep and GABA 

Article 3 – about how sleep loss affects behaviour and emotions

Article 4 – a review on many articles about the link between sleep deprivation and emotional reactivity and perception

Bear et al., 2006. Neuroscience – Exploring the Brain. s.l.:Lippincott Williams & Wilknins 

Rosenzweig et al., 2010. Biological Psychology – An Introduction to Behavioural, Cognitive and Clinical Neuroscience. 6th edition. Sinauer Associates Inc.,U.S., pg. 380-401

Both images by Gabriel Velichkova

Emotions and the brain

Posted on by Iasmina Hornoiu

Once upon a time, I promised I was going to write an article about how emotions affect our decision-making and why it is actually important not to ignore the feelings we have in certain situations…For several, unexplainable reasons I kept postponing this idea, and for that I am very sorry. Having said that, there is no better way of making up for this than to finally keep my promise. So, here we go!

I think I should start off with a small mention: emotions and feelings are distinct things, according to neuroscientist Joseph LeDoux. As he well puts it: “…feelings are what happen when we become consciously aware that our brain is reacting to some significant stimulus,” while it is possible that some brain structures, such as the amygdala “respond to emotional stimuli without the organism being aware of the stimulus.”

In order to achieve a better understanding of what the process of forming emotions involves, scientists talk about emotional experience and emotional expression. The latter refers to body manifestations and behaviours in response to certain stimuli, for example changes in facial expression, heart rate, sweating, skin conductance etc. It has been a subject of debate for several decades whether emotional experience or emotional response is the one responsible for formation of the other, or that they act independently. It is now believed that different emotions depend on specific parts of the brain and are determined by different neural circuits.

But why should we care about emotions in the first place? Some of you might find it strange, but emotions are intensely interconnected with reasoning and decision-making. And no, I don’t mean that they impair the process of making the right decision, it’s actually quite the opposite: most of the times we need emotions in order to be able to do what is best for us in a certain situation.

An interesting case: Phineas Gage 

A man who has gone down in history for surviving a terrible accident at the work place, but maybe mostly because of his importance in understanding the role of emotions in decision-making, is a late 19th century foreman, Phineas Gage. He had been hired as a foreman on a railroad construction site in Vermont and one of his tasks was to sprinkle explosive powder into blasting holes. This sounds like a dangerous thing to do, but Gage was regarded as one of the best people in this field: he was said to be very efficient, energetic, balance-minded, tenacious, a smart and successful business man etc.

One moment of carelessness dramatically changed his life forever, and at the same time had a huge impact on the way scientists began to think of emotions. The powder exploded and a tamping iron entered Gage’s head under his left eye, passing through his left frontal lobe, and exited the skull, leaving a hole which measured more than 9 cm in diameter.

Gage survived, but he “was no longer Gage”, as his friends and acquaintances used to say. Apart from losing vision in his left eye, the man had no motor or sensory deficits, he could hear, touch, sense, walk and talk. It was his personality that was completely changed. He became capricious, irreverent, impatient, and behaved as if he did could not predict, nor care about any professional or personal failure. He was soon fired and found different jobs over time, most of which were related to the accident and the iron rod, which had turned him into some sort of freak.

Some explanations and brain functions

The limbic system is probably the first to come to mind if you refer to brain areas involved in emotions. It consists of structures around the thalamus or in the temporal lobe, such as the amygdala, the hypothalamus, the limbic cortex, the cingulate gyrus, the fornix, the corpus callosum etc. Each one of these structures is involved in specific types of emotion and in triggering certain behaviours or responses through the autonomic nervous system. For example, the amygdala is linked to fear and aggression. Different regions (nuclei) in the amygdala are associated certain functions, so that both emotional expression and experience require the amygdala in order to be formed. Projections from amygdala are sent to the hypothalamus, which determines the autonomic response, the brain stem for behavioural reaction and the cerebral cortex, which is involved in emotional experience. The amygdala is also thought to play a role in enhanced emotional memory.

Regulation of specific emotional behaviours depending on the limbic system is facilitated by one of the major neurotransmitters, serotonine. Neurones containing serotonin originate in the brain stem (in the Raphe nuclei) and send projections to the hypothalamus. Serotonine is associated with a decrease in aggressive behaviour, but at the same time is involved in dominance, as proven by studies in rhesus monkeys.

The Papez Circuit (named after the neurologist James Papez who came up with the idea of an “emotional system”) is composed of interconnected anatomical structures (many of which are part of the limbic system) that link emotional expression and emotional experience together. Papez proposed that the cingulate cortex determines emotional experience, while the major structure involved in emotional expression is the hypothalamus. 

Below I have inserted a diagram showing the Papez Circuit, based on information from Bear et al. Note that the hippocampus is now thought to have less importance in the process of emotion formation.

The Papez Circuit

The discussion above does not fully explain what happened in the case of Phineas Gage. There is much more to emotion than that! Given the fact that the iron rod severely affected Gage’s frontal lobe, we should definitely focus our attention on this structure, too. The frontal lobe and the prefrontal cortices are involved in planning, reasoning, social behaviour, motivation, defining our personalities etc. Damage to these regions, especially to the ventromedial prefrontal cortices, results in decision-making impairment. While the intelligence and the other body functions remain intact, the patient who has suffered the damage is no longer able to exhibit normal social behaviour. The patient becomes emotionless and this lack of emotions and self motivation makes them incapable of making the right decisions.

If instead of the ventromedial prefrontal cortices, another region of the prefrontal cortices is affected, there is a very strong possibility that the patient’s intellectual abilities are compromised, along with their ability to form emotions. This region is called the dorsolateral prefrontal cortices. The person with a damage in this brain area would encounter severe difficulties when it comes to operations on numbers, words, space etc.

Another brain structure involved in the process of emotion forming is located in the right hemisphere. If the somatosensory cortices of this area are injured, the result would be similar to what can be seen in the case of a damaged ventral prefrontal cortex, but there is something more…the processes of basic body singling are also disrupted. This can be observed in patients suffering from anosognosia, a disease in which the patient is unaware and denies their disability.

I have tried to comprise a lot of information and simplify things as much as possible. If you managed to get here with both eyes open, I couldn’t be happier. Hopefully, you can see now why we should also “think with our hearts” when we need to decide about a certain situation…because the “heart” is somewhere in the brain and it knows better than us what we need to do.

For further information:

Antonio Damasio,1995. Decartes’ Error. Vintage Books

Bear et al., 2006. Neuroscience – Exploring the Brain. s.l.:Lippincott Williams & Wilknins pp. 564-581

Article about Phineas Gage

Image by Isuru Priyaranga 

Yourself…and decision-making!

Posted on by Iasmina Hornoiu

I recently came across a very interesting post on Facebook, written in Romanian. This post especially caught my attention first of all because it had been made by a group very dear to me, Yourself; secondly, the topic was exactly the one I was thinking about for my next article. It’s about the role of emotions in decision-making. To be honest, this is something I’ve been studying for a while and I’ve been struggling to synthesise the main ideas for an article. But this post had it all: it is clear, concise, easy to read and definitely not boring.

I now have a very good starting point for my article. So in the meantime, I thought, why not translate it? 🙂

“When we were small it was easy to write letters to Santa, because we knew exactly what we wanted and we made choices with no difficulty. But as we grew older, things got a bit more complicated; the further we navigate the path to maturity and complexity of life, the more it becomes a challenge to make up our minds.

Why is it sometimes so hard to make choices?; Why do we get anxious and agitated whenever we have to face the impossibility of making a decision? Perhaps it comes down to the fact that the process of decision-making involves many options, and taking the variables into consideration involves both reason and emotions.

The logical process of decision-making is based on determining the value of each option. We often try to rule out as many emotional aspects as possible, to detach from them, and to evaluate each alternative in a logical, almost mathematical, way.

On the other hand, decisions we make in particular emotional states, such as when we are angry or extremely happy, are said to be “in the heat of the moment”. So, which one of these two alternatives represents the best way of making a decision?

Antonio Damasio, a Neuroscience specialist, performed studies on people with deficits in the prefrontal cortex (which is responsible for decision-making, among other cognitive functions) and the cortical structures involved in generating emotions. These people would hardly make even the simplest decisions, such as choosing between fish or chicken as a meal, going shopping, taking a walk etc. He also noted that these individuals were able to reasonably evaluate the consequences of their choices and objectively analyse the alternatives, but could not or it was extremely difficult to make any decision, no matter how simple they were.

Going back to the idea of multiple variables in decision-making, emotions are part of these variables and it is important to acknowledge their role in this process. Life is full of choices and decisions, and we have to face them all. Moreover, if our decisions are based on strong moral values, we will find the necessary means to deal with any potential challenge, regardless the final choice (which we could be quite uncertain about).”

I hope you enjoyed it! 🙂

Drawing by James Dowinton

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