Büyük Sistemlerde Çalışmanın Zihinsel Riskleri

Büyük sistemlerde çalışmak çeşitli felaketlerle sonuçlanabilecek ciddi bir iştir.  Ben bunlardan en iyi olasılıkla sinirsel patlama ya da daha kötüsü psikotik problemlerle sonuçlanabilecek üçü üzerinde duracağım.

Working on Large Systems is a serious commitment which may end up with various disasters.  I will mention only three of the mental risks that may cause burn-out in the simplest possibilities or serious psychotic problems.

 1-       Kronik stress’te norepinephrine – cortisol etkileşimi ve ani moral bozucu durumlar.

“Akut stress altında-“döğüş ya da kaç”mayı düşünürken- hypothalamus bolca corticotropin-serbest bırakan hormon üretir, stres hormonu cortisol miktarında ani bir yükselmeyi tetikleyerek bağışıklığı, belleği, enerji ve cardiovascular işlevleri arttırır.  Strese neden olan şey geçtikten sonra, DHEA hormonu, neuropeptide Y ve diğer biokimyasallar içeri hücum eder ve dengeyi yeniden inşa ederek hipertansiyon gibi belirtileri hafifletir.  Akut olarak, bu dengeleyiciler bir görev ile duygusal bağlantıya paralel olarak öğrenmeyi genişletir.

1-       Norepinephrine – cortisol interaction in chronic stress and sudden demotivation cases.

“Under acute stress—think “fight or flight”—the hypothalamus churns out corticotropin-releasing hormone, prompting a sharp rise in the stress hormone cortisol, which enhances immunity, memory, energy and cardiovascular function. Once the stressor has passed, the hormone DHEA, neuropeptide Y and other biochemicals rush in, restoring equilibrium and easing symptoms, such as hypertension. Acutely, these mediators, along with emotional engagement with a task, may enhance learning.

Fakat, stres sürekli(chronic) ise, cortisol sağlığı yıpratır.  Bağışıklığın baskı altına alınması, hipertansiyon, kemik minerali kaybı, adele kaybı ve metabolik rahatsızlıklar bunu takip eder.[1]”

But when stress is chronic, cortisol erodes health. Immune suppression, hypertension, bone mineral loss, muscle wasting and metabolic disorders ensue.[1]”

“Stress hormonlarının kronik(sürekli) yüksek salgılanması beyin fonksiyonlarını kötü etkiler, özellikle belleği.  Çok miktarda cortisol beynin yeni bellek ayırmasını, veya halen var olan bellek hatıralarına erişmesini engelleyebilir.[2]”

“Chronic over-secretion of stress hormones adversely affects brain function, especially memory. Too much cortisol can prevent the brain from laying down a new memory, or from accessing already existing memories.[2]”

Ünlü beyin araştırmacısı Robert M. Sapolsky sürekli stresin hippocampuste hasar oluşturabileceğini göstermiştir, hippocampus öğrenme ve bellek için merkezi olan limbic beynin bir parçasıdır.  Suçlular ise adrenal bezleri tarafından stres sırasında salgılanan “glucocorticoid”’lerdir.  Onlar çoğunlukla corticosteroidler ya da cortisol olarak bilinirler.[2]”

“The renowned brain researcher, Robert M. Sapolsky, has shown that sustained stress can damage the hippocampus , the part of the limbic brain which is central to learning and memory. The culprits are "glucocorticoids," a class of steroid hormones secreted from the adrenal glands during stress. They are more commonly know as corticosteroids or cortisol.[2]”

“Aşırı cortisol düşünmeği ya da uzun-dönem hatıralara erişmeği zorlaştırır.  Ciddi krizlerde insanlar bu yüzden aptallaşır ve tereddütlere düşer.  Zihinleri boşalır çünkü “hatlar kesiktir”.  Fire exit – yangın çıkışının bile nerede olduğunu hatırlayamazlar, örneğin.[2]”

“Excessive cortisol can make it difficult to think or retrieve long-term memories. That's why people get befuddled and confused in a severe crisis. Their mind goes blank because "the lines are down." They can't remember where the fire exit is, for example.[2]”

Norepinephrine cortisol’ün kötü yan tesirlerini dengeler.  Ağır yük altında çalışan yüksek motivasyonlu bir insan eğer motivasyonu aniden yok eden bir şeyle karşılaşırsa potansiyel bir felaketle karşılaşabilir.

Norepinephrine kaynağı aniden durur ve beyni aniden yalnızca çok miktarda cortisol ile karşılaşır.  Büyük sistemlerde hem kişisel hem de yönetimsel açıdan motivasyon kontrolünün önemli olmasının nedeni budur.  Bir yönetici ağır yük altında yüksek motivasyonla çalışan bir elemanı kolaylıkla ve kalıcı şekilde yaralayabilir.  Ödül bekleyen kişiyi cezalandırın.    Zihinsel olarak  iş yapamaz ve kovulmuş olur.

Norepinephrine balances the bad sideeffects of cortisol.  A highly motivated person working under heavy load goes into a potential disaster if something happens that removes the motivation abruptly.  Norepinephrine supply suddenly stops and his brain faces an abundant amount of cortisol alone.  This is why motivation control both by individuals and the management is so important on large systems.  A manager can easily and permanently hurt an employee who is working under heavy load with high motivation.  Punish the person who expects a reward.  He will be mentally sacked.

2-       Kindling yani sinir bağlantılarının sürekli stress altında bilinçsiz olarak gelişmesi.  Bu kişinin belirli bir neden olmadan stres hissetmesi durumunu açıklayabilir.  Ya da kişinin en ufak bir stress altında kaldığında geçmişe ilişkin önemli bir stress kaynağı olayı hatırlaması şeklinde görülebilir.

2-       Kindling namely growth of neural paths unconsciously under continuous stress.  This may explain the situations when somebody feels stress without any reason or remembers a stressful experience at the moment he feels stress about an important problem triggered by some other and simple reason.

“Kindling beyin bağlantılarını yeniden kurar…  beyin küçük zararlı uyarılara yanıt olarak kendini yeniden şekillendirir…  Kindling bir çeşit öğrenme olarak belirir, fakat muhakemeden bağımsız olarak var olabilen bir öğrenme…  Hastalık, bir kere ortaya çıktığında, giderek küçülen uyarılara yanıt verebilir ve, zamanla, uyarıdan tamamen bağımsız olarak tetiklenir.  Düzensizlik zamanla daha karışık bir hal alır.[3]”

"Kindling rewires the brain. … the brain reshapes itself anatomically in response to small noxious stimuli. … Kindling appears to be a kind of learning, but a learning that can occur independent of cognition. … Illness, once expressed, can become responsive to ever smaller stimuli and, in time, independent of stimuli altogether. The expression of the disorder becomes more complex over time[3]."

Bir sinir bağlantı yolu kullanıldığında güçlenir.  Ne kadar çok kullanılırsa o kadar güçlenir.  Çocukluk hatıralarımız bu şekilde tazelenir[3].

If a neural path is used it gets stronger.  The more it is used the stronger it becomes.  Our childhood memories are renewed like this[3].

“Zamanla, tekrarlanan stresli tecrübeler, yalnız laf olarak değil, gerçekten, karakter olarak hassas kişilerin sinir sistemlerini değiştirir.  Hayvanlar üzerinde yapılan araştırmalar, bir fareye küçük bir şok verildiğinde, belirgin bir tepki vermediğini; beş ardışık gün boyunca benzer stres yapıcılara maruz kaldığında, stres tepkisi gösterdiğini; yedi veya sekiz gün maruz kaldığında, farenin bir atak geçirdiğini, ve daha sonra bu ‘kindled hayvanın’ çok küçük veya hiç provakasyon olmadan atak geçirdiğini göstermiştir[3].

“Over time, repeated stressful experiences can literally, not just figuratively, alter the nervous systems of the temperamentally vulnerable. Animal research has shown that when a rat is given a small shock, it shows no marked reaction; when exposed to such stressors for five consecutive days, it shows signs of the stress response; when exposed for seven or eight days, the rat has a seizure, and thereafter this 'kindled' animal will seize with little or no provocation[3].

Duyarlılık açısından yaralanabilir bir kişi moral bozucu bir uyarı ile sürekli bombalanırsa, Gold der ki,

harekete geçen genler stres yanıtının hücresel bileşenleri ile ilgili olanlardır[3].”

When a temperamentally vulnerable person is constantly bombarded with upsetting stimuli, Gold says, the genes that get turned on are those involved in the cellular components of the stress response[3]."

“Amydolaid işlevi genişletecek, Hippocampal işlevi aksatacak büyük bir travmatik stres edici oluştuğunu kabul ediniz.  Daha sonraki bir noktada, benzer bir ortamda, tasa, otonomik durum, ajite ve korku hissediyorsunuz ve bunun için belirli bir neden yok-çünkü hippocampus aracılığı ile ilgili olayın hatıralarını toparlamadığınız halde amygdala-aracılığı ile oluşan autonomic patika yolları kesinlikle olayı hatırlamaktadır[3].”

"Suppose a major traumatic stressor occurs, of a sufficient magnitude to disrupt hippocampal function while enhancing amygdaloid function. At some later point, in a similar setting, you have an anxious, autonomic state, agitated and fearful, and you haven't a clue why—this is because you never consolidated memories of the event via your hippocampus while your amygdala-mediated autonomic pathways sure as hell remember[3]."

3-       Zayıf bir sosyal yaşam sürmenin(Yalnızlığın) beyin üzerindeki etkisi.

3-       The effect of living an asocial life on the brain.

Daha çok sayıda ve karmaşıklıkta sosyal ilişkilere sahip olan kişilerin daha büyük hacimde amygdala sahibi oldukları ispat edilmiştir[4,5].

It is proved that people who have a larger number and more social relations have bigger amygdala volumes[4,5].

Zayıf ve yetersiz sosyal ilişkileri olan kişiler küçük amygdala sahibi olmak ve böylece ilgili zihinsel problemler riski ile karşı karşıyadır.  “Şizofreni hastalarının ölümünden sonra yapılan incelemeler amygdala ve diğer orta limbic yapılarda önemli miktarda küçülme bulmuştur(Bogerts 1984; Bogerts et all., 1985)[6]”.

People who have few and weakly inadequate social relations are at the risk of getting smaller amygdala and hence they are faced with the risk of getting related mental problems:  “Postmortem studies of  schizophrenic patients have found significant amygdala volume reductions as well as of other medial lymbic structures (Bogerts 1984; Bogerts et all., 1985)[6]”.

 

REFERENCES:

[1] FOCUS, Harvard Medical School; The Science of Resiliency, May 5, 2011.

Bruce McEwen, a professor of neuroendocrinology at the Rockefeller University, The Embattled Brain.

Linking the nervous and endocrine systems, biochemical mediators regulate the effects of stress, which are exacerbated by health-related behaviors such as inactivity or poor diet. Under acute stress—think “fight or flight”—the hypothalamus churns out corticotropin-releasing hormone, prompting a sharp rise in the stress hormone cortisol, which enhances immunity, memory, energy and cardiovascular function. Once the stressor has passed, the hormone DHEA, neuropeptide Y and other biochemicals rush in, restoring equilibrium and easing symptoms, such as hypertension. Acutely, these mediators, along with emotional engagement with a task, may enhance learning.

But when stress is chronic, cortisol erodes health. Immune suppression, hypertension, bone mineral loss, muscle wasting and metabolic disorders ensue. Within the hippocampus and amygdala, seats of memory and emotion, dendrites shrink and synapses vanish, McEwen has shown. Cognitive function declines, depression sinks in, the immune system weakens, and metabolism goes awry. In a study of medical students preparing for board exams, McEwen’s collaborators found that higher levels of perceived stress predicted poor mental flexibility and reduced functional connectivity in the prefrontal cortex.

The good news: These ill effects are reversible, McEwen said. Regular exercise returns the hippocampus to normal size and improves memory, for example, while mindfulness training reduces the amygdala’s volume and curbs anxiety. Many adult diseases could be prevented by reducing toxic stress in utero and in early childhood, he said.

[2] Resources for Science Learning, The Franklin Institute, “The Human Brain”, Unisys.

“Attack of the Adrenals”-A Metabolic Story

The ambulance siren screams it’s warning to get out of the way. You can’t move your car because you’re stuck in a bumper-to-bumper traffic jam that reaches as far as the eye can see. There must be an accident up ahead. Meanwhile the road construction crew a few feet from your car is jack-hammering the pavement. You are about to enter the stress zone.

"Attention all parasympathetic forces. Urgent. Adrenal gland missile silos mounted atop kidneys have just released chemical cortisol weapons of brain destruction. Mobilize all internal defenses. Launch immediate counter-calm hormones before hippocampus is hammered by cortisol."

Hormones rush to your adrenal glands to suppress the streaming cortisol on its way to your brain. Other hormones rush to your brain to round up all the remnants of cortisol missles that made it to your hippocampus. These hormones escort the cortisol remnants back to Kidneyland for a one-way ride on the Bladderhorn. You have now reached metabolic equilibrium, also known as homeostasis.

...

Stress and Memory

Chronic over-secretion of stress hormones adversely affects brain function, especially memory. Too much cortisol can prevent the brain from laying down a new memory, or from accessing already existing memories.

The renowned brain researcher, Robert M. Sapolsky, has shown that sustained stress can damage the hippocampus , the part of the limbic brain which is central to learning and memory. The culprits are "glucocorticoids," a class of steroid hormones secreted from the adrenal glands during stress. They are more commonly know as corticosteroids or cortisol .

During a perceived threat, the adrenal glands immediately release adrenalin. If the threat is severe or still persists after a couple of minutes, the adrenals then release cortisol. Once in the brain cortisol remains much longer than adrenalin, where it continues to affect brain cells.

Cortisol Affects Memory Formation and Retrieval

Have you ever forgotten something during a stressful situation that you should have remembered? Cortisol also interferes with the function of neurotransmitters, the chemicals that brain cells use to communicate with each other.

Excessive cortisol can make it difficult to think or retrieve long-term memories. That's why people get befuddled and confused in a severe crisis. Their mind goes blank because "the lines are down." They can't remember where the fire exit is, for example.

Why We Lose Our Memory

Stress hormones divert blood glucose to exercising muscles, therefore the amount of glucose – hence energy – that reaches the brain's hippocampus is diminished. This creates an energy crisis in the hippocampus which compromises its ability to create new memories.

That may be why some people can't remember a very traumatic event, and why short-term memory is usually the first casualty of age-related memory loss resulting from a lifetime of stress.

Cortisol and Temporary Memory Loss-Study

In an animal study, rats were stressed by an electrical shock, and then made to go through a maze that they were already familiar with. When the shock was given either four hours before or two minutes before navigating the maze, the rats had no problem. But, when they were stressed by a shock 30 minutes before, the rats were unable to remember their way through the maze.

This time-dependent effect on memory performance correlates with the levels of circulating cortisol, which are highest at 30 minutes. The same thing happened when non-stressed rats were injected with cortisol. In contrast, when cortisol production was chemically suppressed, then there were no stress-induced effects on memory retrieval.

According to James McGaugh, director of the Center for the Neurobiology of Learning and Memory at the University of California, Irvine, "This effect only lasts for a couple of hours, so that the impairing effect in this case is a temporary impairment of retrieval. The memory is not lost. It is just inaccessible or less accessible for a period of time."¹²

Cortisol and the Degenerative Cascade

Normally, in response to stress, the brain's hypothalamus secretes a hormone that causes the pituitary gland to secrete another hormone that causes the adrenals to secrete cortisol. When levels of cortisol rise to a certain level, several areas of the brain – especially the hippocampus – tell the hypothalamus to turn off the cortisol-producing mechanism. This is the proper feedback response.

The hippocampus, however, is the area most damaged by cortisol. In his book Brain Longevity, Dharma Singh Khalsa, M.D., describes how older people often have lost 20-25% of the cells in their hippocampus, so it cannot provide proper feedback to the hypothalamus, so cortisol continues to be secreted. This, in turn, causes more damage to the hippocampus, and even more cortisol production. Thus, a Catch-22 "degenerative cascade" begins, which can be very difficult to stop.

Cortisol and Brain Degeneration-Study

Studies done by Dr. Robert M. Sapolsky, Professor of Neurology and Neurological Sciences at Stanford University, showed that lots of stress or exposure to cortisol accelerates the degeneration of the aging hippocampus.

And, because the hippocampus is part of the feedback mechanism that signals when to stop cortisol production, a damaged hippocampus causes cortisol levels to get out of control – further compromising memory and cognitive function. The cycle of degeneration then continues. (Perhaps similar to the deterioration of the pancreas-insulin feedback system.

Cortisol Levels During Human Aging-Study

The study was titled "Cortisol levels during human aging predict hippocampal atrophy and memory deficits". A third of the 60 volunteers, who were between ages 60 and 85, had chronically high cortisol levels, a problem that seems to be fairly common in older people.¹³

 

The size of the hippocampus averaged 14% smaller in one group and showed high and rising cortisol levels, compared to a group with moderate and decreasing levels. The small hippocampus group also did worse at remembering a path through a human maze and pictures they'd seen 24 hours earlier and – two tasks that use the hippocampus.

Reference of Stress on the Brain:
12. Nature, Aug 20, 1998
13. Nature Neuroscience, May 1998.

[3] MyBrainNotes™.com, Subcortical Brain Structures, Stress, Emotions, and Mental Illness

Kindling and stress—how experience affects the brain:

Is it possible that chronic stress, through a process called kindling, can create hard-wired, hypersensitive neural networks capable of dictating and automating symptoms from a wide range of instinctual behavior patterns? In his video course, Biology and Human Behavior: The Neurological Origins of Individuality, 2nd edition, Robert M. Sapolsky examines how communication between neurons is strengthened as a result of experience. When the dendritic spines of neurons are stimulated rapidly, the synapses between the communicating neurons become "hyper-responsive or potentiated" due to chemical changes within the neural environment. Subsequently, less stimulation is necessary to again prod the neuron to fire—the moment when an electrical signal bursts through the neuron's axon, prompting release of chemical messengers called neurotransmitters into the synapse between neurons, often increasing the likelihood that other neurons will fire in a sort of chain reaction. In other words, Sapolsky says, the neuron's "action potential" is increased. What's called "long-term potentiation" is thus the basis for learning and memory, possibly including injurious forms of learning such as post-traumatic stress disorder (PTSD).

In Listening to Prozac: A Psychiatrist Explores Antidepressant Drugs and the Remaking of the Self (1993), Peter D. Kramer writes, "Kindling rewires the brain. … the brain reshapes itself anatomically in response to small noxious stimuli. … Kindling appears to be a kind of learning, but a learning that can occur independent of cognition. … Illness, once expressed, can become responsive to ever smaller stimuli and, in time, independent of stimuli altogether. The expression of the disorder becomes more complex over time."

In "Psychosomatic disease and the 'visceral' brain: Recent developments bearing on the Papez theory of emotion" (1949), Paul D. Maclean theorized about the kindling process. "It is possible that if a certain electrical pattern of information were to reverberate for a prolonged period or at repeated intervals in the neuronal circuit, the nerve cells (perhaps, say, as the result of enzymatic catalysis in the dentritic processes at specific axone-dendritic junctions) would be permanently 'sensitized' to respond to this particular pattern at some future time. Such a mechanism would provide for one variety of enduring memory in a way that is remotely analogous to a wire recorder. These hypothetical considerations suggest how oft-repeated childhood emotional patterns could persist to exert themselves in adult life."

As MacLean suggests in using the term visceral, certain reactions are not embedded in language and intellect, they are more like "gut feelings" that can remain in primordial memory systems and that can be strengthened through kindling. Winifred Gallagher explains kindling in an article in The Atlantic Monthly, "How We Become What We Are" (September 1994). Gallagher writes:

Over time, repeated stressful experiences can literally, not just figuratively, alter the nervous systems of the temperamentally vulnerable. Animal research has shown that when a rat is given a small shock, it shows no marked reaction; when exposed to such stressors for five consecutive days, it shows signs of the stress response; when exposed for seven or eight days, the rat has a seizure, and thereafter this 'kindled' animal will seize with little or no provocation. Experiments of this kind are of course not done with people, but Philip Gold and other neuroscientists now think that in human beings, too, by triggering a cascade of chemical reactions, serious chronic stress, particularly in early life, causes changes in the way genes within a brain cell function, permanently altering the neuron's biology. Because they require a particular type of input to turn on or off, only some of a neuron's thousands of genes, each of which is involved in some aspect of cellular structure or communication, are activated at any given moment. When a temperamentally vulnerable person is constantly bombarded with upsetting stimuli, Gold says, the genes that get turned on are those involved in the cellular components of the stress response."

I contend that neurotransmission in the amygdalae and their target structures is sometimes kindled to generate dopamine-driven behaviors aimed at solving problems including restoring order, control, and most importantly–confidence. Under normal circumstances, this could be construed as a survival instinct. Under extreme stress, however, especially when an outlet for pent-up energy is not available, these behaviors may turn into obsessions or compulsions. We will discuss such neurotransmission in greater detail in Part 3 of MyBrainNotes.com. For now, I would like to point out that in Monkeyluv and Other Essays on Our Lives as Animals (2005), Robert M. Sapolsky describes how monkeys release dopamine in anticipation of a food reward. They get most excited when a light first comes on signaling that they may now perform a learned task and upon completion, will receive food. Their excitement does not peak when the food finally appears; it peaks well before that point. Sapolsky writes, "It's about the anticipation of reward. It's about mastery and expectation and confidence."

...

Another example of kindling, which we discuss above, is the effects of stress on the hippocampi. In his 1995 New York Times article titled, "Severe Trauma May Damage the Brain as Well as the Psyche," Daniel Goleman explains that studies in rats and primates suggest that glucocorticoids are the culprit. Goleman quotes Robert Sapolsky, who explains that glucocorticoids "may be neurotoxic to the hippocampus at the massive levels that are released under extreme stress or during trauma. I'm talking about the levels you would see in a zebra running from a lion, or a person fleeing a mugger—a real physical life-and-death crisis—if it is repeated again and again as time goes on."

If the glucocorticoids released during extreme stress and trauma damage the hippocampi, it is no wonder that, according to Sapolsky in Why Zebras Don't Get Ulcers, "there is atrophy of the hippocampus in long-term depression. The atrophy emerges as a result of the depression (rather than precedes it), and the longer the depressive history, the more atrophy and the more memory problems."

Sapolsky points to the work of psychologists Martin Seligman and Steven Maier who exposed animals to "pathological amounts" of stress. "The result is a condition strikingly similar to a human depression." Sapolsky explains that it is "repeated" stress that generates depressive symptoms combined with "a complete absence of control on the part of the animal." In other words, the animal has no outlets that can be used to vent frustration. "When it comes to what makes for psychological stress, a lack of predictability and control are at the top of the list of things you want to avoid," Sapolsky writes.

Sapolsky calls attention to the work of Joseph LeDoux of New York University, "who pretty much put the amygdala on the map when it comes to anxiety." In a way that only he can do, Sapolsky sums up the paradox between severe, traumatic stress and its effect on the hippocampi versus the amygdalae. "Suppose a major traumatic stressor occurs, of a sufficient magnitude to disrupt hippocampal function while enhancing amygdaloid function. At some later point, in a similar setting, you have an anxious, autonomic state, agitated and fearful, and you haven't a clue why—this is because you never consolidated memories of the event via your hippocampus while your amygdala-mediated autonomic pathways sure as hell remember."

[4] Kevin C Bickart1, Christopher I Wright2,3, Rebecca J Dautoff2,3, Bradford C Dickerson2–4 & Lisa Feldman Barrett2,3,5; Nature America  Nature-Neuroscience, Amygdala volume and social network size in humans, 2010

We found that amygdala volume correlates with the size and complexity of social networks in adult humans. An exploratory analysis of subcortical structures did not find strong evidence for similar relationships with any other structure, but there were associations between social network variables and cortical thickness in three cortical areas, two of them with amygdala connectivity. These findings indicate that the amygdala is important in social behavior.

...

 In this study we examined whether amygdala volume varies with individual variation in the size and complexity of social groupings within a single primate species, humans. In 58 healthy adults (22 females; mean age M = 52.6, s.d. = 21.2, range = 19–83 years) with confirmed absence of DSM-IV Axis I diagnoses and normal perform­ance on cognitive testing, we examined social network size and com­plexity with two subscales of the Social Network Index (SNI9).

 Linear regression analyses revealed that individuals with larger and more complex social networks had larger amygdala volumes (Fig. 1).

[5] Wikipedia, the free encyclopedia; Amygdala

Social interaction

Amygdala volume correlates positively with both the size (the number of contacts a person has) and the complexity (the number of different groups to which a person belongs) of social networks.^[41][42] Individuals with larger amygdalae had larger and more complex social networks. They were also better able to make accurate social judgments about other persons' faces.^[43] It is hypothesized that larger amygdalae allow for greater emotional intelligence, enabling greater societal integration and cooperation with others.^[44]

[6] Ivone-CastroVale, Lilianna de Sousa, Maria Amelia Tavares, Rui Coelho; PSICOSSOMATICA 2002, Knowing the Amydala: Its Contribution to Psychiatric Disorders

Postmortem studies of  schizophrenic patients have found significant amygdala volume reductions as well as of other medial lymbic structures (Bogerts 1984; Bogerts et all., 1985).

...

Measures of amydala volumes with MRI of 46 schizophrenics compared to 60 normal controls and 27 bipolar subjects found right amygdala volumes smaller in schizophrenia and left amygdala volumes smaller in bipolar disorder (Pearlson et all., 1997) .