BIOPSYCHOLOGY OF EMOTION, STRESS AND HEALTH

Here are some theories about emotion in summarize form:

Darwin’s The Expression of Emotions in Man and Animals was the first major event in the study of the biological bases of emotion.Darwin believed emotions evolved from behaviors that indicated what an animal would do next in a given situation; that when these behaviors were advantageous to the animal

The James-Lange Theory was the first attempt to explain the physiological bases of emotion; suggests that emotion-inducing stimuli are received and interpreted by the brain, which triggers visceral changes ( organ changes in the abdomen or thorax) that subsequently trigger the experience of emotion

Canon-Bard Theory is alternative theory based on the idea that emotional stimuli evoke visceral and emotional responses that are independent of one another.

Neither theory is entirely correct; emotions can be induced by stimuli that cannot elicit a peripheral, visceral response (e.g., patients suffering from a spinal cord transection), but visceral responses can often induce an emotional state in the absence of any obvious eliciting stimuli (e.g., a racing heartbeat and increased respiration can produce a feeling of fear in the absence of an eliciting stimuli). Bard reported that decorticate cats (without cortex) responded with unusual aggression to the slightest provocation; often this behavior was not directed at any specific topic. Bard concluded that the hypothalamus is critical for the performance of these aggressive behaviors, which he called sham rage; he also believed that the cortex normally inhibited and directed these aggressive displays. This theory of hypothalamic function was followed by Papez’s proposal of a limbic system that controlled the expression of emotions by connections with the hypothalamus and mediated the perception of emotions by connections with the cortex. This was supported by Kluver-Bucy syndrome - damage to the amygdala (part of the limbic system) resulting patients who are fearless, hypersexual, and inclined to explore objects with mouth.

Stress – reaction to harm to threat

Stressors – stimuli that cause stress

Chronic psychological stress – most clearly linked to ill health

In the short-term stress is adaptive, in the long-term it is maladaptive

Activation of the anterior-pituitary adrenal-cortex system. Selye neglected the role of the sympathetic nervous system. All common psychological stressors are associated with high levels of glucocorticoids, epinephrine, and norepinephrine.

hormones and sex

Sex hormone-binding globulin (SHBG) is a glycoprotein that binds to sex hormones, to be specific, testosterone and estradiol. Other steroid hormones such as progesterone, cortisol, and other corticosteroids are bound by transcortin.

Testosterone and estradiol circulate in the bloodstream, bound mostly to SHBG and to some degree bound to serum albumin. Only a small fraction is unbound, or "free," and thus biologically active and able to enter a cell and activate its receptor. The SHBG inhibits the function of these hormones. Thus, bioavailability of sex hormones is influenced by the level of SHBG. SHBG has a higher affinity for Dihydrotestosterone than for Testosterone or for Estradiol, making it essential in women for regulating the bio-availability of Dihydrotestosterone.

SHBG is produced mostly by the liver and is released into the bloodstream. Other sites that produce SHBG include the brain, uterus, testes, and placenta. Testes-produced SHBG is called androgen-binding protein. The gene for SHBG is located on chromosome 17.

SHBG levels appear to be controlled by a delicate balance of enhancing and inhibiting factors. Its level is decreased by high levels of insulin and insulin-like growth factor 1 (IGF-1) (see:milk). Also, high androgen and transcortin levels decrease SHBG, whereas high growth hormone, estrogen, and thyroxine levels increase it.

However, recent evidence suggests that it is the liver's production of fats that reduces SHBG levels,^[2][3] not any direct effect of insulin and specific genetic mechanisms that do this have been found.

Conditions with low SHBG include polycystic ovary syndrome, diabetes, and hypothyroidism. Conditions with high SHBG include pregnancy, hyperthyroidism, and anorexia nervosa. There has recently been research to link high SHBG levels with breast and testicular cancer as well.

Biopsychology Of Motivation

Hunger and Eating

Many theories of hunger are historically discussed from the biological component. Cannon and Washburn (as cited in Coon, 1995) came up with the stomach contraction theory which states that we know we are hungry when our stomach contracts. In the notorious balloon study, Washburn trained himself to swallow a balloon which was attached to a tube, then the balloon was inflated inside of his stomach. When the balloon was inflated, he did not feel hungry. Later this theory was opposed by the fact that people whose stomach was removed still felt hungry. Glucose theory states that we feel hungry when our blood glucose level is low. Bash (as cited in Franken, 1994) conducted an experiment transfusing blood from a satiated dog to a starved dog. The transfusion resulted in termination of stomach contraction in the starved dog, and supported the glucose theory. But as LeMagnen (as cited in Kalat, 1995) suggests that blood glucose level does not change much under normal conditions. Insulin theory states that we feel hungry when our insulin level increases suddenly in our bodies (Heller, & Heller, 1991). However, this theory seems to indicate that we have to eat to increase our insulin level in order to feel hungry. Fatty acid theory states that our bodies have receptors that detect an increase in the level of fatty acid. Activation of the receptor for fatty acid triggers hunger (Dole, 1956, Klein et al., 1960 cited in Franken, 1994). Heat-Production theory suggested by Brobeck (as cited in Franken, 1994) states that we feel hungry when our body temperature drops, and when it rises, the hunger decreases. This might be explain that we tend to eat more during winter.

Health

Many theories point out that obese people have a strong biological component of hunger and eating. What about people with eating disorders? What is the mechanism of hunger and eating for people with eating disorders? There are mainly three kinds of eating disorders; Binge Eating, Anorexia Nervosa, and Bulimia. Binge eating is characterized by one's eating a very large amount of food until she or he feels uncomfortably full. This binge eating is done when one is not hungry. According to the DSM-VI, Anorexia Nervosa has two types; restricting type, and binge-eating/purging type (American Psychiatric Association, 1994). Anorexia Nervosa restricting type is when one extremely restricts food intake, and it is not followed by binge-eating or purging behavior. On the other hand, Anorexia Nervosa binge-eating/purging type was described as one engaged in purging and binge-eating regularly. A common symptom of Anorexia is one's putting her or himself on self-starvation to avoid feeling fat or gaining weight. Although people with this disorder weigh far below normal, they still think they are overweight. Eventually they are at risk of losing their lives due to malnutrition.

People with this disorder still feel hungry, yet they cannot eat because they are too afraid of gaining weight. Physiological causes of this disease are not yet clear, although there are some findings showing a connection with serotonin and norepinephrine. The learned component of Anorexia cannot be ignored. Studies show that there is more Anorexia in westernized cultures than other cultures, (e.g., Suematsu, 1986), because the social value of slimness pushes people to be thinner. Cognitively, these people have a distorted body image of themselves, and dissatisfaction with their own body image, which is influenced by the cultural value of slimness, and leads to eating disorders (Mumford, Whitehouse, & Choudry, 1992).

Bulimia Nervosa is a condition of binge eating followed by purging and use of laxatives (American Psychiatric Association, 1994). Unlike Anorexia, people with this disorder are normal or above weight. Psychologically, having quilt and shame are common symptoms among people with Bulimia. Unlike anorexic people who put absolute control over restricted eating, bulimic people cannot control their eating. The physiological cause of Bulimia is still unclear. Psychologically, Bulimia is said to be linked to depression and anxiety, but clear evidence of causation has not yet been found. Cognitively, people with Bulimia are said to be motivated to escape from reality by binging. It is possible that those people were given food by their caretakers to lift their mood in their childhood. Like Anorexia, cultural learning that one needs to be thin to be accepted may also contribute to the cause.

Reference:

http://www.csun.edu/~vcpsy00h/students/hunger.htm

Learning, Memory and Amnesia

Memory and learning
are so closely connected that people often confuse them with each other. But the specialists who study them consider them two distinct phenomena.
These specialists define learning as a process that will modify a subsequent behavior.

Memory, on the other hand, is the ability to remember past experiences.

You learn a new language by studying it, but you then speak it by using your memory to retrieve the words that you have learned. Memory is essential to all learning, because it lets you store and retrieve the information that you learn. Memory is basically nothing more than the record left by a learning process. Thus, memory depends on learning. But learning also depends on memory, because the knowledge stored in your memory provides the framework to which you link new knowledge, by association. And the more extensive your framework of existing knowledge, the more easily you can link new knowledge to it.

Memory system is divided into three functions for storage

• Sensory Memory: The sensory memory retains an exact copy of what is seen or heard (visual and auditory). It only lasts for a few seconds, while some theorize it last only 300 milliseconds. It has unlimited capacity.
• Short-Term Memory (STM) - Selective attention determines what information moves from sensory memory to short-term memory. STM is most often stored as sounds, especially in recalling words, but may be stored as images. It works basically the same as a computer's RAM (Random Access Memory) in that it provides a working space for short computations and then transfers it to other parts of the memory system or discards it. It is thought to be about seven bits in length, that is, we normally remember seven items. STM is vulnerable to interruption or interference.
• Long-Term Memory - This is relatively permanent storage. Information is stored on the basis of meaning and importance.

Amnesia
is a profound memory loss which is usually caused either by physical injury to the brain or by the ingestion of a toxic substance which affects the brain. In addition, the memory loss can be caused by a traumatic, emotional event.

People with amnesia have difficulty learning new information, and/or they have difficulty recalling previously learned information. They may be disoriented and confused. Their memory deficit causes problems for them either at work, in school, or in social settings. Sometimes the memory loss is severe enough to necessitate a supervised living situation.

Psychotherapy can be helpful for people whose amnesia is caused by emotional trauma. For instance, hypnosis may help some patients/clients recall forgotten memories.

Sometimes it is appropriate to administer a drug called Amytal (sodium amobarbital) to people suffering from amnesia. The medicine helps some people recall their lost memories.

Reference:
http://thebrain.mcgill.ca/flash/d/d_07/d_07_p/d_07_p_tra/d_07_p_tra.html
http://www.nwlink.com/~donclark/hrd/learning/memory.html
http://www.apa.org/topics/learning/index.aspx
http://www.athealth.com/Consumer/disorders/Amnesia.html

Schizotypal Personality Disorder

Schizotypal Personality Disorder

it is a condition characterized by acute discomfort with, and reduced capacity for, close relationships as well as by cognitive or perceptual distortions and eccentricities of behavior. This disorder is only diagnosed when these behaviors become persistent and very disabling or distressing. This disorder should not be diagnosed if the distrust and suspiciousness occurs exclusively during the course of Schizophrenia, a Mood Disorder With Psychotic Features, or another Psychotic Disorder or if it is due to the direct physiological effects of a neurological (e.g., temporal lobe epilepsy) or other general medical condition.

A disorder characterized by eccentric behaviour and anomalies of thinking and affect which resemble those seen in schizophrenia, though no definite and characteristic schizophrenic anomalies have occurred at any stage. There is no dominant or typical disturbance, but any of the following may be present:

• - Inappropriate or constricted affect (the individual appears cold and aloof);
• - Behaviour or appearance that is odd, eccentric, or peculiar;
• - Poor rapport with others and a tendency to social withdrawal;
• - Odd beliefs or magical thinking, influencing behaviour and inconsistent with subcultural norms;
• - Suspiciousness or paranoid ideas;
• - Obsessive ruminations without inner resistance, often with dysmorphophobic, sexual or aggressive contents;
• - Unusual perceptual experiences including somatosensory (bodily) or other illusions, depersonalization or derealization;
• - Vague, circumstantial, metaphorical, overelaborate, or stereotyped thinking, manifested by odd speech or in other ways, without gross incoherence;
• - Occasional transient quasi-psychotic episodes with intense illusions, auditory or other hallucinations, and delusion-like ideas, usually occurring without external provocation.

TREATMENT


As with most personality disorders, schizotypal personality disorder is best treated with some form of psychotherapy. Individuals with this disorder usually distort reality more so than someone with Schizoid Personality Disorder.

Psychotherapy

As with Delusional Disorder and Paranoid Personality Disorder, the clinician must exercise care in therapy to not directly challenge delusional or inappropriate thoughts. A warm, supportive, and client-centered environment should be established with initial rapport. As with Avoidant Personality Disorder, the individual lacks an adequate social support system and usually avoids most social interactions because of extreme social anxiety. The patient often reports feelings of being "different" and not "fitting in" with others easily, usually because of their magical or delusion thinking. There is no simple solution to this problem. Social skills training and other behavioral approaches which emphasize the learning of the basics of social relationships and social interactions may be beneficial.

While individual therapy is the preferred modality at the onset of therapy, it may be appropriate to consider group therapy as the client progresses. Such a group should be for this specific disorder, though, which may be difficult to form or find in smaller communities.

Building a trusting relationship with a therapist may help people with schizotypal personality disorder begin to trust other interpersonal relationships.

Treatment can be more effective when family members are involved. Seeking professional counseling as a group may help reduce fighting or emotional distance in the home. Family therapy may also offer the affected person a support structure and a boost in morale.

Cognitive therapy. This type of therapy can help people with schizotypal personality disorder identify and change distorted thought patterns. For example, this type of therapy may help a person with schizotypal personality disorder uncover — and change — confused ideas about what goes on in interpersonal exchanges.

Other treatments, such as group therapy and social skills training, can help you to manage symptoms. Family therapy may also help.

Counseling is often beneficial for people with schizotypal personality disorder. Counseling sessions focus on helping you gain insight into your personality disorder and changing your behavior.

Self-help

There are not any self-help support groups or communities that we are aware of that would be conducive to someone suffering from this disorder. Such approaches would likely not be very effective because a person with this disorder is likely to be mistrustful and suspicious of others and their motivations, making group help and dynamics unlikely and possibly harmful.

Medication

There's no specific drug treatment for schizotypal personality disorder. However, doctors may prescribe antidepressant or antipsychotic medications to help relieve associated conditions, such as anxiety, depression or other mood disorders. For example, prescription medications such as risperidone (Risperdal) and olanzapine (Zyprexa) may help reduce distorted thinking.

Currently there is no medication available specifically for this condition. You may be prescribed an antipsychotic drug called pimozide (Orap) to treat distorted thinking. Other drugs that may be used include risperidone (Risperdal) , haloperidol (Haldol) , and olanzapine (Zyprexa).

Comorbidity

When we say comorbidity, it is either the presence of one or more disorders (or diseases) in addition to a primary disease or disorder, or the effect of such additional disorders or diseases.

In response to stress, individuals with this disorder may experience very brief psychotic episodes (lasting minutes to hours). If the psychotic episode lasts longer, this disorder may actually develop into Brief Psychotic Disorder, Schizophreniform Disorder, Delusional Disorder or Schizophrenia. Individuals with this disorder are at increased risk for Major Depressive Disorder. Other Personality Disorders (especially Schizoid, Paranoid, Avoidant, and Borderline) often co-occur with this disorder.

Reference:

http://www.mayoclinic.com/health/schizotypal-personality-disorder/DS00830/DSECTION=treatments-and-drugs

http://www.thirdage.com/hc/c/schizotypal-personality-disorder-treatment

http://psychcentral.com/disorders/sx33t.htm

http://www.mentalhealth.com/dis/p20-pe03.html

http://en.wikipedia.org/wiki/Comorbidity

Brain Damage

Brain damage is brain injury that is either mild, moderate or severe and brain damage can involve either open head or closed head injury.

Open head injury occurs when the skull is displaced or fractured by an outside force and closed head injury occurs when the skull is not displaced or fractured by an outside force. Some of the different types of brain damage include concussion, contusion, diffuse axonal injury, penetration damage, anoxic injury and hypoxic injury.

Hypoxic brain damage occurs when the level of oxygen is not sufficient enough to allow for normal body functioning. Stagnant hypoxia is also referred to as hypoxic ischemic brain injury and ischemic insult brain injury and the damage to the brain is caused by inadequate blood pressure and/or blood flow. Anoxic brain damage differs from hypoxic brain damage in that no oxygen at all reaches the brain. In anemic anoxia, brain damage is caused from the lack of oxygen in the blood. In anoxic anoxia, the lack of oxygen to the brain causes brain damage.

Penetration brain damage is caused by an object such as a bullet or knife that brings the object or parts of the object and bone, hair and skin into the brain. Diffuse axonal brain damage occurs when the skull moves too fast for the brain such as in a car accident or in Shaken Baby Syndrome. A contusion is a bruise formed by blood on the brain due to head injury. Surgery to remove the contusion may be required if the bruise is large.

A concussion is a sudden impact to the brain that affects the blood vessels and may sometimes cause a fatal blood clot. A loss of consciousness may or may not result in a concussion. Both blood vessels and nerves in the brain may be damaged and the concussion may take months or even years to heal.

Both open head and closed head brain damage may involve brain swelling, but closed head brain swelling is usually more dangerous as the brain has less room to enlarge in. The Glascow Coma Scale (GCS) is used to assess the degree of brain damage severity in terms of neurological damage. Mild brain damage may involve a short loss of consciousness or just some confusion, while moderate brain damage usually involves longer periods of unconsciousness and confusion. Severe brain damage may involve unconsciousness or a coma that will remain for several months. The physical and cognitive affects also vary in degree in cases of mild, moderate and severe brain damage.

Development of NERVOUS SYSTEM

In vertebrates, landmarks of embryonic neural development include the birth and differentiation of neurons from stem cell precursors, the migration of immature neurons from their birthplaces in the embryo to their final positions, outgrowth of axons from neurons and guidance of the motile growth cone through the embryo towards postsynaptic partners, the generation of synapses between these axons and their postsynaptic partners, and finally the lifelong changes in synapses which are thought to underlie learning and memory.^[56]

All bilaterian animals at an early stage of development form a gastrula, which is polarized, with one end called the animal pole and the other the vegetal pole. The gastrula has the shape of a disk with three layers of cells, an inner layer called the endoderm, which gives rise to the lining of most internal organs, a middle layer called the mesoderm, which gives rise to the bones and muscles, and an outer layer called the ectoderm, which gives rise to the skin and nervous system.^[57]

Human embryo, showing neural groove

Four stages in the development of the neural tube in the human embryo

In vertebrates, the first sign of the nervous system is the appearance of a thin strip of cells along the center of the back, called the neural plate. The inner portion of the neural plate (along the midline) is destined to become the central nervous system (CNS), the outer portion the peripheral nervous system (PNS). As development proceeds, a fold called the neural grooveneural tube, whereas the future PNS appears as two strips of tissue called the neural crest, running lengthwise above the neural tube. The sequence of stages from neural plate to neural tube and neural crest is known as neurulation. appears along the midline. This fold deepens, and then closes up at the top. At this point the future CNS appears as a cylindrical structure called the

In the early 20th century, a set of famous experiments by Hans Spemann and Hilde Mangold showed that the formation of nervous tissue is "induced" by the underlying mesoderm. For decades, though, the nature of the induction process defeated every attempt to figure it out, until finally it was resolved by genetic approaches in the 1990s. Induction of neural tissue requires inhibition of the gene for a so-called bone morphogenetic protein, or BMP. Specifically the protein BMP4 appears to be involved. Two proteins called Noggin and Chordin, both secreted by the mesoderm, are capable of inhibiting BMP4 and thereby inducing ectoderm to turn into neural tissue. It appears that a similar molecular mechanism is involved for widely disparate types of animals, including arthropods as well as vertebrates. In some animals, however, another type of molecule called Fibroblast Growth Factor or FGF may also play an important role in induction.

Induction of neural tissues causes formation of neural precursor cells, called neuroblasts.^[58] In drosophila, neuroblasts divide asymmetrically, so that one product is a "ganglion mother cell" (GMC), and the other is a neuroblast. A GMC divides once, to give rise to either a pair of neurons or a pair of glial cells. In all, a neuroblast is capable of generating an indefinite number of neurons or glia.

As shown in a 2008 study, one factor common to all bilateral organisms (including humans) is a family of secreted signaling molecules called neurotrophins which regulate the growth and survival of neurons.^[59] Zhu et al. identified DNT1, the first neurotrophin found in flies. DNT1 shares structural similarity with all known neurotrophins and is a key factor in the fate of neurons in Drosophila. Because neurotrophins have now been identified in both vertebrate and invertebrates, this evidence suggests that neurotrophins were present in an ancestor common to bilateral organisms and may represent a common mechanism for nervous system formation.

Reference:

http://en.wikipedia.org/wiki/Nervous_system#Development