Emotions and the brain

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 

Mechanisms of schizophrenia

It took me a while to figure out whether to divide this article into two parts or to sum up everything in one long, possibly tedious reading. Honestly, I still don’t know, so I’ll just start writing and we shall see what it turns out to be.

I’m sure you’ve all heard of schizophrenia – the disease of thought disorder, or know people who suffer from it. But only a few actually understand what it is about.

No wonder scientists have been struggling to develop efficient treatments for schizophrenia; not only is it largely uncommon (1% of the world’s population is affected), but also its causes are usually unknown. Scientists generally refer to schizophrenia as a psychiatric disease involving a progressive decline in functioning, which begins in early adolescence and persist throughout the patient’s life. Due to its heterogenous symptoms and multiple possible causes, there are many hypotheses that intend to explain what triggers schizophrenia and how it develops.

In spite of the fact that is it a genetic disorder, the environment and external factors (such as viral infections during the intrauterine and infant period) may be crucial to the development of schizophrenia. The symptoms have been divided into two categories. The positive symptoms include thought disorder, hallucinations, delusions, disorganised speech etc., whereas the negative symptoms are characterised by poverty of speech, reduced expression or emotion, memory impairment, anergia, abulia etc. In addition, the brains of schizophrenics show structural macroscopic abnormalities (for instance, the enlarged ventricles and the shrinkage of the surrounding brain tissue), as well as microscopic changes, such as the dysregulation of dysbindin gene in the formation of abnormal dendritic filopodia. There are three types of schizophrenia, according to its symptoms: paranoid schizophrenia – auditory hallucinations, delusions, strong belief of being chased by powerful people; disorganized schizophrenia – reduced emotions and lack of emotional expressions, incoherent speech (mostly negative symptoms); catatonic schizophrenia – impairment of movement, usually immobility and catatonia, bizarre grimacing (this is similar some of the symptoms of hysteria, which has been described as a sexually related and later on, as a psychiatric disorder up until the beginning of the 20th century).

But enough with the boring general details! Let’s get to the fun part: The monoamine hypothesis of schizophrenia! Here we are going to talk about two very important neurotransmitters in the central nervous system: dopamine and glutamate. The second one is the main excitatory neurotransmitter in the brain. There are four main types of glutamate receptors: AMPA, NMDA, kainate and mGluRs. It has been demonstrated that reduced activity of the NMDA receptors can result in some of the negative symptoms of schizophrenia (lack of social behaviour, catatonia).

Dopamine is the metabolic precursor of another neurotransmitter, noradrenaline (norepinephrine). But there is a lot more to dopamine and its roles in the brain than this. There are four main dopaminergic pathways: the mesolimbic pathway – related to the “reward” system and significance; it has its roots in the ventral tegmental area and projects to the nucleus accumbens (in the ventral striatum) and the limbic system; the mesocortical pathway – involved in cognition and motivation; the tuberoinfundibular pathway – roles in lactation; these dopamine neurones originate in the hypothalamus; the nigrostrial pathway – involved in movement planning and connects the substantia nigra (midbrain) to the striatum.

Schizophrenia and another mental illness, a neurodegenerative one, Parkinson’s disease, are also linked to dopamine. When it comes to schizophrenia, it seems that the mesocorticolimbic pathways have more influence on its onset: the ‘positive’ symptoms appear to be triggered by dopaminergic hyperactivity in the mesocorticolimbic system. At the same time, hypoactivity of dopamine is this region is the cause of ‘negative’ symptoms. Nevertheless, it has been discovered that overexpression of the dopamine receptor D2 (DRD2) gene in the striatum also reduces motivational behaviour in mice, therefore mimicking psychotic ‘negative’ symptoms. Similar findings show that increased density of dopamine D2 receptor in the striatum, along with lower thalamic density of this receptor appear to induce divergent thinking, which is associated with schizophrenia.  

All these changes may account for the abnormalities that we see in “mad” people. It seems that we are so fragile, given that often small chemical and physical disruptions can trigger something as big and terrifying as schizophrenia. Imagine hearing, seeing, feeling, smelling things everyone says are not real (schizophrenics often have multiple hallucinations: auditory, visual, gustatory, tactile, olfactory). But to you they are so real and disturbing! Many schizophrenics even hear their own thoughts as if they are coming from the outside and therefore believe that everyone knows what’s in their heads. Imagine having the constant feeling that someone is after you (paranoia) or being certain that you are dead (the Cotard’s Syndrome) or that your husband has an affair (the Othello Syndrome).

I think this topic can never be fully covered and we would spend days talking about schizophrenia, so this article should better come to an end. As I am sure you have lots of questions and comments, don’t be shy and post anything you think it’s relevant to what has been discussed above. Hope you enjoyed this reading.

For further information: 

Bear et al., 2006. Neuroscience – Exploring the Brain. s.l.:Lippincott Williams & Wilknins, pp. 679-684

de Manzano et al., 2010. Thinking Outside a Less Intact Box; Thalamic Dopamine D2 Receptor Densities Are Negatively Related to Psychometric Creativity in Healthy Insividuals. Public Library of Science

Jia et al.,  2014. The Schizophrenia Susceptibility Gene Dysbindin Regulates Dendritic Spine Dynamics. The Journal of Neuroscience, Oct.pp. 34-41

Kandel et al., 2011. Modeling Motivational Deficits in Mouse Models of Schizophrenia: Behavior Analysis as a Guide for Neuroscience. Behavior Processes, pp. 149-156

Kolb et al., 1996. Fundamentals of Human Neuropsychology. 4th Edition ed. s.l.:W.H. Freeman and Company

Image by Damaris Pop