Atrial Fibrillation

Atrial fibrillation is a cardiac arrhythmia in which the heart atria (upper chambers) tremble instead of beating effectively in synchronic contraction. Atrial fibrillation can be identified by taking a pulse and observing that the heartbeats do not occur at regular intervals. However, a conclusive indication of atrial fibrillation is the absence of P waves on an electrocardiogram (ECG or EKG), which are normally present when there is a coordinated atrial contraction at the beginning of each heart beat. Risk increases with age, with 8% of people over 80 having AF.

In atrial fibrillation, the normal electrical impulses that are generated by the sinoatrial node are overwhelmed by disorganized electrical impulses that originate in the atria and pulmonary veins, leading to conduction of irregular impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat which may occur in episodes lasting from minutes to weeks, or it could occur all the time for years. Atrial fibrillation usually becomes a chronic condition, which leads to a small increase in the risk of death. The probability of developing atrial fibrillation increases with age and three to five percent of people over 65 suffer from atrial fibrillation.

Right Atrial Appendage

The right atrial appendage is a small conical muscular pouch that is attached to the right atrium of the heart. Its margins have a dentated edge. The right atrial appendage projects from the upper and front part of the sinus forward and toward the left side, overlapping the root of the aorta. The right atrium, along with the right atrial body, is lined with pectinate muscles that form a network of hills and furrows that give it a trabeculated surface. It is believed that tachycardia to emerge from the right atrial appendage.

Intraventricular Septum

Interventricular septum, also called ventricular septum, is the thick muscular wall which divides the right ventricle from the left ventricle of the heart. The ventricular septum is runs obliquely backward and to the right, and is curved with the convexity toward the right ventricle: its margins correspond with the anterior and posterior longitudinal sulci. The greater portion of it is thick and muscular and constitutes the muscular ventricular septum. Its upper and posterior part is thin and fibrous and separates the aortic vestibule from the lower part of the right atrium and upper part of the right ventricle; it is called the membranous ventricular septum.

Right Ventricle

The right ventricle is one of the four chambers of the heart. The right ventricle is connected to the right atrium, from which it receives deoxygenated blood through the tricuspid valve. It contracts during sistole to pump the blood out into the pulmonary artery through the pulmonary valve and pulmonary trunk. The right ventricle is triangular in shape, extending from the right atrium to near the apex of the heart.

The heart is divided into four chambers: two atria, which are situated in the upper half of the heart, right and left atria; and two ventricles, right and left. The ventricles are not connected to one another but to their respective atrium. The right ventricle is located in the lower right quarter of the heart and is separated from the left ventricle by the interventricular septum.

Coronary Sinus

The coronary sinus is a large vein which is formed by several smaller veins that converge into one larger blood vessel, opening into the right atrium of the heart. Collecting blood from the myocardium, the coronary sinus is the drainage channel of the deoxygenated blood of heart. It runs across in the groove situated on the posterior surface of the heart, between the left atrium and left ventricle. The coronary sinus collects blood from the small, middle, great and oblique cardiac veins. It also receives blood from the left marginal vein and the left posterior ventricular vein.

The coronary sinus opens into the atrium, between the inferior vena cava and the atrial-ventricular opening. It returns the blood from the substance of the heart, and is protected by a semicircular fold of the lining membrane of the atrium, the coronary valve. The sinus, before entering the atrium, is considerably dilated - nearly to the size of the end of the little finger. Its wall is partly muscular, and at its junction with the great coronary vein is somewhat constricted and furnished with a valve consisting of two unequal segments.

Heart Murmurs

Heart murmurs are abnormal sounds which are produced as a result of blood flowing turbulently, producing audible noise. Murmurs may be present in normal hearts without any heart disease. These types of murmurs, often referred to as innocent murmurs, usually cause no trouble for the patient. Murmurs may also be the result of various problems, such as narrowing or leaking of valves, or the presence of abnormal passages through which blood flows in or near the heart. Such murmurs, known as pathologic murmurs, should be evaluated by an expert. Although most murmurs do not affect a person's health at all, some heart murmurs are caused by deffective heart valves. Murmurs also can be caused by conditions such as pregnancy, fever, and thyrotoxicosis.

Angina Pectoris

Angina pectoris is a severe chest pain which is caused by a lack of blood and hence oxygen supply to the myocardium, generally due to obstruction or spasm of the coronary arteries. This lack of blood supply is called ischemia. Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries. The Latin word angina means "infection", and the Latin pectus "chest". There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle. Major risk factors for angina include cigarette smoking, diabetes, high cholesterol, high blood pressure, sedentary lifestyle and family history of premature heart disease.

Most patients suffering form angina pectoris complain at the beginning of chest discomfort rather than actual pain, such as a pressure, heaviness, tightness, squeezing, burning, or choking sensation. Apart from chest discomfort, anginal pains may also be experienced in the epigastrium (upper central abdomen). Ischemia of the myocardium arises when the the heart muscles receive insufficient blood and oxygen to function normally. This inadequate perfusion of blood and the resulting reduced delivery of oxygen and nutrients is directly correlated to blocked or narrowed blood vessels.

Mitral Regurgitation

Mitral regurgitation is the abnormal blood backflow from the left ventricle back into the left atrium of the heart every time the left ventricle contracts to pump the blood out into the aorta artery during sistole. "Regurgitation" means "backflow". This heart condition is caused by mitral valve prolapse, which is the reversion of one or both of the mitral valve leaflets into the wrong side (the left atrium). If mitral regurgitation is severe, people have difficulties in breathing, but mild regurgitation might not need treatment. Severe regurgitation could cause the accumulation of fluid in the lungs. There are two types of mitral regurgitation: 1) chronic, which develops slowly as the person gets older; 2) acute mitral regurgitation, which develops quickly is often life-threatening.

The most common cause of primary mitral regurgitation is myxomatous degeneration of the valve, which is more common in males and in advanced age people. It is due to a genetic abnormality that results in a defect in the collagen that makes up the mitral valve. This causes a stretching out of the leaflets of the valve and the chordae tendineae. The elongation of the valve leaflets and the chordae tendineae prevent the valve leaflets from fully coapting when the valve is closed, causing the valve leaflets to prolapse into the left atrium, thereby causing mitral regurgitation.

Mitral Stenosis

Mitral stenosis is a heart condition in which the mitral valve orifice is abnormally too narrow for an efficient blood flow. The mitral valve opens during left ventricular diastole to let blood flow from the left atrium (upper left chamber) to the left ventricle (lower left chamber). When a person suffers from mitral stenosis, the mitral valve does not open completely; in order to pump the same amount of blood the left atrium needs a higher pressure than normal to overcome the increased gradient. As a result, the left atrium swells when pressure builds up, increasing the risk of blood flowing back into the lungs; this could cause pulmonary edema.

Usually mitral stenosis is caused by rheumatic fever. But less common causes of mitral stenosis are calcification of the mitral valve flaps, and congenital malformation of the heart valves.

Endocarditis

Endocarditis is an inflammation of the endocardium, which is the inner lining of the heart. Endocarditis occurs when bacteria in the bloodstream attach to damaged areas of the heart, such as the valves and chordae tendinae. It is characterized by a microcolonies of bacteria and fungi, and inflammatory cells. If left untreated, endocarditis can damage the heart valves and lead to life-threatening cardiac complications.

The symptoms of endocarditis are: weakness, tiredness, fever, night sweat, and heart murmur. The heart conditions that could cause endocarditis include: heart damage (from Rheumatic Fever, for example), congenital heart defects, intravenous drug use, dental extraction, etc.

As heart valves do not receive direct blood irrigation, white blood cells cannot directly reach the valves through the bloodstream. So, if bacteria and fungi settle to a damaged valve surface, forming a vegetation, the host immune response is blunted. The lack of blood supply to the valves also has implications on treatment, since drugs also have difficulty reaching the infected valve. Usually, blood flows smoothly through these valves. Wehn the heart valves have been damaged by rheumatic fever, the risk of bacteria attachment is increased.

Mitral Valve Prolapse

Mitral valve prolapse is a valvular condition of the heart. It occurs when a mitral valve flap turns into the left atrium during systole, causing blood to flow back from the left ventricle to the left atrium. This happens when one or both flaps (or leaflets) of the mitral valve are abnormally thickened. Mitral valve prolapse can cause mitral regurgitation, congestive heart failure, and endocarditis. Mitral valve prolapse is classified as classic and nonclassic.

In order to be able to effectively diagnose mitral valve prolapse, one has to resort to echocardiography, which uses ultrasound to visualize the mitral valve. Early studies wrongly estimated a prevalence of 38% among healthy teenage males. Nevertheless, using echocardiography, it has been discovered that it really affects only 2-3% of the general population, and it is most often diagnosed in people aged 20-40 years. Some people may inherit the condition, which is associated with connective tissue disorders like Marfan syndrome.

Cardiac Conduction System

The cardiac conduction system is the electrical conduction which makes the heart contract rhythmically to pump the blood out into the rest of the body. It is composed of sinoatrial node, the Bachmann's bundle, the atrioventricular node, the bundle of His, and the cardiac excitation wave pathway. The normal electrical conduction in the heart allows the impulse that is generated by the sinoatrial node of the heart to be spread to the myocardium, which contracts after stimulation. The ordered stimulation of the myocardium allows efficient contraction of the heart, pumping the blood throughout the body.

Substantial atrial to ventricular delay allows the atria to completely empty their contents into the ventricles; simultaneous contraction would cause inefficient filling and backflow. After contracting, the heart must relax to fill up again. Sustained contraction of the heart without relaxation would be fatal, and this is prevented by a temporary inactivation of certain ion channels.

The miocardium cells has some similarities both to neurons and skeletal muscle cells, and also have important unique properties. Like a neuron (nerve cell), a given myocardial cell has a negative membrane potential when at rest. Stimulation above a threshold value induces the opening of voltage-gated ion channels and a flood of cations into the cell. The positively charged ions entering the cell cause the depolarization characteristic of an action potential. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels and release of Ca2+ from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca2+ causes muscle contraction. After a delay (the absolute refractory period), potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization to the resting state.

Atrioventricular Node

The atrioventricular node is a part of the cardiac conducting system and functions as an electrical relay station located between the right atrium and the right ventricle. The atrioventricular (AV) node coordinates heart rate. It electrically connects the atria and the ventricles. The AV node is an area of specialized tissue between the atria and the ventricles of the heart, specifically in the posteroinferior region of the interatrial septum near the opening of the coronary sinus, which conducts the normal electrical impulse from the atria to the ventricles. The AV node is quite compact (~1 x 3 x 5 mm). It is located at the center of Koch's Triangle—a triangle enclosed by the septal leaflet of the tricuspid valve, the coronary sinus, and the membraneous part of the interatrial septum.

The atrioventricular node is activated when a wave of excitation spreads out from the sinoatrial node through the atria along specialized conduction channels. The atrioventricular node delays impulses by approximately 0.12s. This delay in the cardiac pulse ensures that the atria have ejected their blood into the ventricles first before the ventricles contract.

Right Atrium

The right atrium is one of four chambers of the heart. There are two atria in the heart, the right and the left atrium, which are not communicated with one another. The right atrium gets deoxygenated blood from the superior and inferior vena cava, pumping it into the right ventricle through the tricuspid valve. The right auricular appendix is attached to it.

In the walls of the right atrium, next to the entrance of the superior vena cava, is the sinoatrial node, whose cells generates electrical impulses that begin the cardiac contractions. The right atrium is irrigated by the right coronary artery.

Sinoatrial Node

The sinoatrial node is the impulse-generating tissue located in the upper part of right atrium of the heart, and thus the generator of sinus rhythm. It is an importan part of the cardiac conduction system which controls the heart rate. The sinoatrial node is a group of modified cardiac myocytes (cells), which are situated on the wall of the right atrium, near the entrance of the superior vena cava. Although they have some contractile filaments, they do not contract.

All of the heart's myocytes can generate the electrical impulses that trigger cardiac contraction, but it is the sinoatrial node that initiates it, as it generates impulses slightly faster than the other areas with pacemaker potential. Because cardiac myocytes, like all muscle cells, have refractory periods following contraction during which additional contractions cannot be triggered, their pacemaker potential is overridden by the sinoatrial node.

In the absence of extrinsic neural and hormonal control, cells in the sinoatrial node will naturally discharge at about 60-100 beats/minute. Because the sinoatrial node is responsible for the rest of the heart's electrical activity, it is sometimes called the primary pacemaker. The electrical impulses from the sinoatrial node triggers a sequence of electrical events in the heart to control the orderly sequence of muscle contractions that pump the blood out of the heart.

If the sinoatrial node stopped functioning, a group of cells further down the heart will become the heart's pacemaker. These cells form the atrioventricular node, which is an area between the atria and ventricles, within the atrial septum. The autonomic nervous system controls the firing of the sinoatrial node to trigger the initiation of the cardiac cycle. The autonomic nervous system can transmit a message quickly to the sinoatrial node so it can increase the heart rate to twice normal within only 3 to 5 seconds.

Nucleus Accumbens

The nucleus accumbens is a collection of neurons within the striatum. It plays an important role in reward, laughter, pleasure, addiction, fear, and the placebo effect. Each half of the brain has one nucleus accumbens. It is located where the head of the caudate nucleus and the anterior portion of the putamen meet just lateral to the septum pellucidum. The nucleus accumbens and the olfactory tubercle collectively form the ventral striatum, which is part of the basal ganglia. The nucleus accumbens can be divided into two structures: 1) the nucleus accumbens core; 2) the nucleus accumbens shell. These structures have different morphology and function.

The main neuronal cell type that is found in the nucleus accumbens is the medium spiny neuron. The neurotransmitter produced by these neurons is gamma-aminobutyric acid, one of the main inhibitory neurotransmitters of the central nervous system. These neurons are also the main projection or output neurons of the nucleus accumbens. While 95% of the neurons in the nucleus accumbens are medium spiny GABA-ergic projection neurons, other neuronal types are also found such as large aspiny cholinergic interneurons.

Ventral Tegmental Area

The ventral tegmental area is a group of neurons located close to the midline on the floor of the midbrain. The The ventral tegmental area (VTA) is involved in the drug and natural reward circuitry of the brain, cognition, and motivation. The VTA contains neurons that project to numerous areas of the brain, from the prefrontal cortex to the caudal brainstem and everywhere in between. The ventral tegmental area forwards information to another structure further forward in the brain: the nucleus accumbens. In order to send information to the nucleus accumbens, the VTA uses a neurotransmitter called dopamine.

It is very difficult to distinguish the ventral tegmental area in humans and other primate brains from the substantia nigra and other surrounding nuclei. The VTA is located in the midbrain between the mammilary bodies and the posterior hypothalamus. The pons is situated caudally to the VTA and the substantia nigra is lying laterally to the VTA. The ventral tegmental area has also been shown to process various types of emotion output from the amygdala, where it may also play a role in avoidance and fear-conditioning. In terms of human evolution, the ventral tegmental area is one of the most primitive part of the brain.

Locus Coeruleus

The locus coeruleus is a cluster of neurons in the brainstem which physiologically responds to stress and panic. The locus coeruleus is situated within the dorsal wall of the rostral pons in the lateral floor of the fourth ventricle. It is composed of medium-size neurons. The locus coeruleus gets inputs from other brain regions, primarily: medial prefrontal cortex; nucleus paragigantocellularis,integrates autonomic and environmental stimuli; nucleus prepositus hypoglossi; and lateral hypothalamus, which releases orexin, which is excitatory in the locus coeruleus.

The locus coeruleus is activated by stress, and will respond by increasing norepinephrine secretion, which in turn will increase cognitive function through the prefrontal cortex, increase motivation, activate the hypothalamic-pituitary-adrenal axis, and increase the sympathetic discharge/inhibit parasympathetic tone (through the brainstem).

The locus coeruleus gained prominence in the 1960s when new anatomical approaches revealed it to be the major source of norepinephrine (NE) in brain with projections throughout most central nervous system (CNS) regions, including the cerebral cortex, hippocampus, thalamus, midbrain, brainstem, cerebellum, and spinal cord. The locus coeruleus is densely innervated by fibers that contain opiates, glutamate, gamma-aminobutyric acid,serotonin, epinephrine, and the newly discovered peptide orexin/hypocretin. The sources of these various inputs have not been fully elucidated, though some major inputs have been identified.

Glial Fibrillary Acidic Protein

Glial fibrillary acidic protein is an intermediate filament protein that is specific for astrocytes in the central nervous system. The glial fibrillary acidic protein (GFAP) was first described in 1971; it was discovered that it is a type III IF protein which maps, in humans, to 17q21. It is closely related to its non-epithelial family members, vimentin, desmin, and peripherin, which are all involved in the structure and function of the cell’s cytoskeleton. It is believed that GFAP helps maintain astrocyte mechanical strength, as well as the shape of cells but its exact function remains poorly understood, despite the number of studies using it as a cell marker.

Loss of glial fibrillary acidic protein impairs the schwann cells proliferation and delays nerve regeneration after damage. The GFAP is involved in many cellular functioning processes, such as cell structure and movement, cell communication, and the functioning of the blood brain barrier. It has also been found that GFAP plays a role in mitosis by adjusting the filament network present in the cell. During mitosis, there is an increase in the amount of phosphorylated GFAP, and a movement of this modified protein to the cleavage furrow.

Multiple Sclerosis

Multiple sclerosis is a chronic and disabling disease in which the body's immune response attacks a person's central nervous system, especially the spinal cord and brain. This leads to the demyelination of axons, which transmit the nerve impulses from the neuron body to the dentrites of another. Thus, multiple sclerosis impairs the ability of neurons (nerve cells) in the brain and spinal cord to link up with each other. Neurons communicate with each other via nerve impulses, or electrical signals, through fibers called axons, which are enveloped in a fatty insulating substance called myelin. In multiple sclerosis, the body's own immune system attacks and destroy the myelin, impairing the axons from effiently transmitting these electrical signals.

The term multiple sclerosis refers to scars (scleroses—better known as plaques or lesions) in the white matter of the brain and spinal cord, which is mainly composed of myelin. Although much is known about the mechanisms involved in the disease process, the cause remains unknown. Theories include genetics or infections. Different environmental risk factors have also been found.

The symptoms of this disease may be mild, like numbness in the limbs, or severe, such as paralysis or loss of vision. The progress, severity, and specific symptoms of multiple sclerosis are unpredictable and vary from one person to another. But almost any neurological symptom can appear with the disease; as it progresses, physical and cognitive disability and neuropsychiatric disorder might appear. Disease onset usually occurs in young adults, and it is more common in females.

Although the cause of multiple sclerosis is still not known, scientists believe that it is caused by a combination of several factors. Presently scientists are doing research in the areas of immunology and genetics in an effort to find the cause of the disease. But it is now generally accepted that multiple esclerosis involves an autoimmune process, which is an abnormal response of the body’s immune system that is directed against the myelin in the central nervous system, such as the brain, spinal cord and optic nerves. The exact antigen, or target that the immune cells are sensitized to attack, remains unknown.

Origin of Eukaryotes

One of the most important transitions in the history of life: the origin of cells with a nucleus, which gave rise to every multicellular form of life. The fossil record doesn't tell us much: The earliest fossils that have been proposed to be eukaryotes are only about 2 billion years old, and paleontologists have not yet discovered any transitional forms. Fortunately, living eukaryotes and prokaryotes, cells that lack a nucleus, still retain some clues to the transition, both in their cell biology and in their genomes. By studying both, researchers have made tremendous advances in the past 20 years in understanding how eukaryotes first emerged. A key step in their evolution, for example, was the acquisition of bacterial passengers, which eventually became the mitochondria of eukaryote cells. But some scientists now argue that the genes of these bacteria also helped give rise to other important features of the eukaryote cell, including the nucleus.

The origin of the eukaryote cell was a milestone in the evolution of life, since they include all complex cells and almost all multi-cellular organisms. The timing of this series of events is hard to determine; Knoll (2006) suggests they developed approximately 1.6 - 2 billion years ago. Some acritarchs are known from at least 1650 million years ago, and the possible alga Grypania has been found as far back as 2100 million years ago. Fossils that are clearly related to modern groups start appearing around 1.2 billion years ago, in the form of a red alga, though recent work suggests the existence of fossilized filamentous algae in the Vindhya basin dating back to 1.6 to 1.7 billion years ago. However, biomarkers suggest that at least stem eukaryotes arose even earlier. The presence of steranes in Australian shales indicates that eukaryotes were present 2.7 billion years ago.

RNA trees constructed during the 1980s and 1990s left most eukaryotes in an unresolved "crown" group (not technically a true crown), which was usually divided by the form of the mitochondrial cristae; see crown eukaryotes. The few groups that lack mitochondria branched separately, and so the absence was believed to be primitive; but this is now considered an artifact of long-branch attraction, and they are known to have lost them secondarily.

Depersonalization in psychosis

Depersonalization is a psychological approach that is universally used as a means of dealing with the other when he becomes disturbing, threatening, or tiresome. One no longer allows oneself to be responsive to his feelings and may be prepared to regard him and treat him as though he had no feelings, turning him as if he were a thing, an it. Partial depersonalization of others is extensively practiced in everday life and is regarded as normal if not highly desirable. Everyday life relationship with strangers are based on some partial depersonalizing tendency in so far as one treats the other not in terms of any awareness of who or what he might be in himself but as virtually an android robot playing a role or part in a large machine in which one too may be acting yet another part.

The inner self in the psychotic condition

In the psychotic condition there is a persistent scission, or split, between the self and the body. What the individual regards as his true self is experienced as more or less disembodied, and bodily experience and actions are in turn felt to be part of a false-self system. It is well known that temporary state of dissociation of the self from the body occur in normal people when they are found trapped in a threating situation from which there is no way out; prisoners in concentration camps felt that way. This temporary dissociation is expressed with such thoughts as "this is like a dream"; "this is unreal"; "I can´t believe this is true", or "nothing seems to be touching me". However, in the psychotic condition, this split of self and body (and reality) is constant.

This detachment of the self means that the self is never revealed directly in the individual's expressions and actions, nor does it experience anything spontaneously. The direct and inmediate transactions between the individual, the other, and the world, all come to be meaningless, futile, and false. The psychotic and schizophrenic individual delegates all transactions between himself and the other to a system whithin his being that is not "him". Thus the world is experienced as unreal, and all that belongs to this system is felt to be false and meaningless. The self, therefore, is precluded from having a direct relationship with real thing and real people. When this has happened in patients, one is witness to the struggle which ensues to preserve the self's own sense of its own realness, aliveness, and identity. The frightened and cornered real self relates to the real world of real people through a false self system which he fabricates to put on a front of normality.

What one might call a creative relationship with the other, in which there is mutual enrichment of the self and the other, is impossible, and this interaction is substituted with sterile relationship. The substitution of an interaction with the other results in the individual coming to live in a frightening world in which dread is unmitigated by love. The individual is frightened of the world, afraid that any impingement will be total, will be implosive, penetrative, fragmenting, and engulfing. He is afraid of letting anything of himself go, of coming out of himself, or losing himself in any experience, because he will be depleted, exhausted, emptied, and robbed.

Psychopathy

Individuals who suffer from psychopathy usually show impulsive and antisocial behavior without accompanying anxiety or guilt, and are unable to form lasting and genuine personal relationships. McCord (1964) considered that the distinguishing features of psychopaths were lack of guilt and the inability to love. Buss (1966) listed psychopathic symptoms as the inability to control impulses or delay gratification, the failure to alter punishable behavior, pathological lying, asocial and antisocial behavior, thrill-seeking behavior, poor judgement of behavior, and rejection of authority, discipline and conventions. However, the lack of anxiety does not occur in all psychopaths. Those who lack anxiety have been called, by Karpman in 1941, "primary psychopaths", as distinct from "secondary" psychopaths who show a mixture of symptoms, including neurotic anxiety.

Although psychopaths seem unable to learn to avoid punishment, they do not show learning defect as such, nor do they suffer from memory defect as such. Psychopathic imperviousness to punishment was investigated directly by Painting in 1961. Gough (1948) suggested that psychopaths lack role-playing ability, that is to say, they are unable to regard themselves as part of society or to identify themselves with the viewpoint of other people. This suggestion was supported in a study by Reed and Cuadra who found that student nurses who tended to psychopathy were less able to predict how others would describe them.

Bowlby stressed early maternal deprivation as a source of psychopathy, quoting as evidence the frequency with which psychopaths were found to have been separated from their mother for six months or more in the first five years of their lives. It has also been demonstrated that institutionalized children were retarded socially and intellectually in comparison with fostered children. A psychopath's lack of empathy, his lack of awareness of behavioral cause and effect, and shallow personal relationships, all derive from his early rearing experiences; in particular, from a frequent change of milieu, a loveless environment, or very inconsistent environmental influence.

Psychoanalytic Theory of Schizophrenia

The psychoanalytic theory of schizophrenia usually explains the illness as a regression to the early oral, or adualistic phase of infancy, when the infant's ability to distinguish self and other is considered to be undeveloped. The schizophrenic symptoms of such regression include feelings of depersonalization and loss, phantasies of world dissolution, passivity, and archaic magical thinking.

Sullivan's psychoanalytic theory of schizophrenia was applied by Kantor and Winder in 1959. They elaborated the theory in process-reactive terms; the earlier the developmental stage to which the individual regresses, the more severe the schizophrenia, that is to say, the more it becomes process rather than reactive. In 1962, Goldman subsequently attempted to apply this general theory to specific aspects of regression in schizophrenia, for example, emotional and social behavior. He drew attention to the similarities of infants and schizophrenics in that both express diffuse emotion impulsively and unpredictably, with little stability of any emotional state.

In 1955, Arieti suggested a theory of progressive teleological regression in terms of neurological structure. He considered that when higher nervous centers, that is those developed later in the evolutionary sequence, are paralyzed by anxiety, lower nervous centers would predominate and thus reduce anxiety. The individual's readjustment to this level can not, however, be maintained because it is too deviant from normal functioning, so that further regression and deterioration is often inevitable. Psychoanalysts usually assume that no psychological crisis is ever fully resolved, and that traces of early part-resolved conflicts and partly satisfied needs will always persist into later life.

Symptoms of Schizophrenia

The symptoms of schizophrenia are sometimes subdivided into primary symptoms, which occur in every schizophrenic, and secondary symptoms, which occur only in some schizophrenics and in other kind of patients, too. The primary symptoms of schizophrenia are affective disturbance, such as dull or apathetic emotional reactions, withdrawal or loss of interest in the environment and other people, and thought disturbances. Secondary symptoms include autism or absorption in an inner phantasy world, delusions, hallucinations, and odd behavior such as posturing and grimacing.

Schizophrenic patients often report feelings of depersonalization and perceptual abnormality such as the flatness, remoteness or unreality of their external environment. Depending on the types of schizophrenia, there is good empirical evidence that some schizophrenics experience disturbances of body image. Feelings of depersonalization are not particularly common among schizophrenics, but are common in compulsive depressive patients and in normal individuals under stress. The classification of schizophrenia by symptoms has not been successful, because the symptons overlap and change over time in the life of a patient.

Arieti (1955) distinguished four successive stages in the course of schizophrenia. In the first stage the major symptom is anxiety; in the second, apathy and withdrawal from reality; in the third stage, regressive habits appear and symtoms become blurred; and in the fourth stage, crude primitive habits predominate. However, nowadays modern treatment ensures that few schizophrenic patients pass beyond the second stage.

Types of Schizophrenia

Many investigators divide the schizophrenia into subgroups, which together are referred to as the "schizophrenias. The types of schizophrenia distinguished traditionally are: simple, catatonic, hebephrenic, and paranoid schizophrenia.

Simple schizophrenia is a type of schizophrenia in which the illness usually begins slowly, often in early adolescence. The patient gradually becomes apathetic, less intelligent in his behavior, and is inclined to withdraw from all interaction with his surroundings.

Catatonic schizophrenia has typical phases of stupor, excitement and negativism, and involves a gross deterioration of personal habits, which may degenerate into a near-vegetative form of living.

Hebephrenics show a marked bizarreness and absurdity in their reactions, and, as they deteriorate show increasing disorganization of most psychological functions.

One of the most common types of schizophrenia is paranoid schizophrenia. It typically entails systematic delusions of persecution, and ideas of reference in which the patient reads personal significance into the everyday actions and ordinary speech of others.

These types of schizophrenia are not mutually exclusive, but tend to overlap regarding some symptoms.

Schizophrenia

Schizophrenia is a mental disorder which is characterized by abnormalities in the perception of reality. A schizophrenic patient suffers from distortions in perception, which may affect the senses of sight and hearing, especially causing auditory hallucinations, paranoid delusions, or disorganized speech and thinking with significant social or occupational dysfunction. Schizophrenia derives from Greek and means divided or split mind: "Schizo", divided; "Phrenia", mind. This means that someone who suffers from this mental disease lacks integrity; its mental or cerebral functions and areas are not integrated into one coherent, rational whole.

A schizophrenic person may show auditory hallucinations, delusions, and disorganized and unusual thinking and speech, which range from loss of train of thought and subject flow, with sentences only loosely connected in meaning, to incoherence, known as word salad, in severe cases. Social isolation commonly occurs for a variety of reasons. Impairment in social cognition is associated with schizophrenia, as are symptoms of paranoia from delusions and hallucinations, and apathy or lack of motivation. Whether it is genetic, or caused by a negative early environment, it has been shown that a schizophrenic does not have the frontal lobe fully integrated to the rest of his cerebral cortex. This is caused by two reasons: 1) when blood irrigation in this region of the cerebrum is not effective; 2) when the white matter of the frontal lobe is poorly myelinated and thus inefficient connections between neurons.

Microglia

Microglia are a type of glial cell that are the resident macrophages of the brain, and thus act as the first and main form of active immune defense in the central nervous system (CNS). Microglia constitute 20% of the total glial cell population within the brain. Microglia (and astrocytes) are distributed in large non-overlapping regions throughout the brain and spinal cord. Microglia are constantly moving and analyzing the CNS for damaged neurons, plaques, and infectious agents. The brain and spinal cord are considered “immune privileged” organs in that they are separated from the rest of the body by a series of endothelial cells known as the blood-brain barrier, which prevents most infections from reaching the vulnerable nervous tissue.

When infectious agents cross the blood-brain barrier, microglia cells must react quickly to increase inflammation and destroy the infectious agents before they damage the sensitive neural tissue. Due to the unavailability of antibodies from the rest of the body (few antibodies cross the blood brain barrier due to their large size), microglia must be able to recognize foreign bodies, swallow them, and act as antigen-presenting cells activating T-cells. Since this process must be done quickly to prevent potentially fatal damage, microglia are extremely sensitive to even small pathological changes in the CNS. They achieve this sensitivity in part by having unique potassium channels that respond to even small changes in extracellular potassium.

Microglial cells differentiate in the bone marrow from hematopoietic stem cells, the progenitors of all blood cells. During hematopoiesis, some of these stem cells differentiate into monocytes and travel from the bone marrow to the brain, where they settle and further differentiate into microglia.

Aphasia

Aphasia is an impairment of language. Someone suffering from aphasia has difficulty in producing or comprehending spoken or written language, but the patient may be able to speak but not write, or vice versa, depending on the area and extent of brain damage. Aphasia may also occur with speech disorders such as dysarthria or apraxia of speech, which also result from brain damage.

Aphasia usually results from lesions to the language centers of the brain, such as the Broca's area and the Wernickle's area, and/or the neural pathways between them. These areas are located in the left hemisphere in most people.

Reticular Formation

The reticular formation is a part of the brain that is involved in actions such as awaking/sleeping cycle, and filtering incoming stimuli to discriminate irrelevant background stimuli. It is essential for governing some of the basic functions of higher organisms, and is one of the phylogenetically oldest portions of the brain. The reticular formation is a diffuse group of nerve fibers which is situated inside the brainstem. The superior portion of the reticular formation is called the reticular activating system.

The reticular formation is a poorly-differentiated area of the brain stem, centered roughly in the pons. The reticular formation is the core of the brainstem running through the mid-brain, pons and medulla. The ascending reticular activating system connects to areas in the thalamus, hypothalamus, and cortex, while the descending reticular activating system connects to the cerebellum and sensory nerves.

Reticular Activating System

The reticular activating system is the part of the brain which functions as the center of arousal and motivation. It is the bridge that connects the brain to the spinal cord. The reticular activating system is located in the brain-stem and is part of the reticular formation. Its function is to maintain an alert state in the cerebral cortex and is concerned with arousal.

Pineal Gland

The pineal gland is a small endocrine gland which is located between the two cerebral hemispheres, tucked in a groove where the two rounded thalamic bodies join. It is attached to the roof of the third ventricle near its junction with the mid-brain, developing as an outgrowth from the third ventricle of the brain. The pineal gland secretes melatonin, which is a hormone that affects the modulation of wake/sleep patterns and photoperiodic functions. It is shaped like a tiny pine cone, hence its name.

The pineal gland is about the size of a pea and is reddish-grey. The pineal body consists of a lobular parenchyma of pinealocytes surrounded by connective tissue spaces. The gland's surface is covered by a pial capsule.

Pinealocyte

A pinealocyte is one of the cell of the pineal body. A pinealocyte has long cytoplasmic processes which end in bulbous expansions, resembling the axons of neurons. Pinealocytes are the main cells which make up the pineal gland. These cells secrete melatonin. Pinealocytes have an organelle called the synaptic ribbon, which is a specific marker for pinealocytes. Some of the enzymes of the pinealocytes include 5-HT N-acetyl transferase and 5-hydroxyindole-O-methyltransferase which are used to convert serotonin to melatonin.

Pinealocytes secrete melatonin into capillaries via the long processes. Secretion of melatonin is stimulated by sympathetic innervation from superior cervical ganglion. They also have shorter cytoplasmic processes that connect to adjacent pinealocytes via desmosomes and gap junctions. Pinealocytes have large irregularly shaped nuclei with prominent nucleoli.