Subject and task of psychiatry and narcology, history of development. Organization of help a patient with psychical violations. Features of structure of psychiatric clinic and dispensary. Principles of examination of mentally ill patients.
Methods of psychiatric research. Psychonosology, concept of psychopathology symptom. Syndrome and disease, registers of psychical disorders. General principles of treatment, rehabilitation and examination of psychical diseases and disorders.
Disorders of sensations and perception.Disorders of memory.
Psychiatry is a medical specialty dealing with the prevention, assessment, diagnosis, treatment, and rehabilitation of the mind and mental illness. Its primary goal is the relief of mental suffering associated with symptoms of disorder and improvement of mental well-being. This may be based in hospitals or in the community and patients may be voluntary or involuntary. Psychiatry adopts a medical approach but may take into account biological, psychological, and social/cultural perspectives. Treatment by medication in conjunction with various forms of psychotherapy may be undertaken and has proved most effective in successful treatment. The word ‘psychiatry’ derives from the Greek for “healer of the spirit” (ψυχ– (spirit) + ιατρος (physician)).
Most psychiatric illnesses cannot currently be cured, although recovery may occur. While some have short time courses and only minor symptoms, many are chronic conditions which can have a significant impact on a patients’ quality of life and even life expectancy, and as such may be thought to require long-term or life-long treatment. Effectiveness of treatment for any given condition is also variable from individual to individual.
History
Physicians in Ancient Egypt and Ancient Greece sought to explain and treat mental disturbance, notably melancholy and hysteria, but medieval thought focused on the concept of demonic possession or supernatural spirits.
Egyptian and ancient Middle Eastern influences can be seen, often as they were incorporated into Greek culture. For instance the importance of dreams and dream interpretation. The Judaic tradition, as evidenced in Judaic scripture, saw insanity as the result of heredity, physiology, improper sexual behavior, failure to uphold ritual prescriptions, idleness, but most importantly as a punishment from God directly or through the agency of evil spirits or demons, as in the story of Saul. Those with mental illness appear to have been treated with benevolence, similar to children, but they were often feared and avoided if violent. Laws were instituted for their care and limiting their responsibilities and obligations.
Much of western beliefs about mental functioning can be traced to Greek and Roman sources. As seen through mythology and the Homeric and other epics, mental illness was often seen as directly due to the involvement of the gods in early Greece. Likewise, cures were also seen as coming from the gods. A relationship can be seen in later Greek literature between moral failure and insanity, such as the gods punishing someone for arrogance. There is also a sense of madness as emotional imbalance due to events or trauma. Both of these may be seen in the Greek tragedies. There is an increasing emphasis on achieving a balance between emotions or passions and reason.
Hippocrates
The increasing emphasis oatural knowledge and an equal de-emphasis of the role of the gods occurs in the 5th and 6th centuries B.C. These continue into the theories of Hippocrates in the 4th century B.C. who believed that illness was the result of an imbalance between the four bodily humors: blood, black bile, yellow bile, and phlegm, which correspond to the four basic qualities of matter: heat, cold, moisture, and dryness. A predominance of one element also determined basic character types. He further argued that certain illnesses, especially epilepsy were not divine, but nervous illnesses. Madness was often seen as a disturbance of black bile (melaina chole) or later melancholia. Hysteria was attributed to the movement of the uterus. As a consequence of these beliefs, treatment was aimed at restoring hormonal balance through the use of purgative, vapors, baths, and special diets. These ideas formed the center of much of medicine until the 17th century.
The philosophy underlying these beliefs saw people as endowed with characteristics at birth that needed education and training to be fulfilled. There was an increasing acceptance of natural laws. Passion and immorality were increasingly seen as derived from the interaction of natural laws (physis) and the influence of irrational customs (nomos). For instance Plato (428-348 B.C.) saw the psyche or soul as active and immortal. The psyche had three parts: appetite, reason, and temper. Irrational behavior was seen as an inevitable part of human life, to be overcome by reason. Illness came from a loss of balance between the psyche and the body or soma, or through self-deception. Reason and rational thought are the highest of virtues. Whereas the body was temporary and of secondary importance.
Aristotle
Aristotle (384-322 B.C.) the student of Plato, accepted the humoral theory of Hippocrates, taking it further seeing that bile mediated between the mind and the body. Whereas Platonic ideas emphasized a division between mind/soul and body, Aristotelian ideas recognized more of an interaction between these entities. He also taught knowledge was the direct consequence of the senses, rather than innate or divinely given. This exemplifies the interaction between mind and body. He emphasized experience and empirical knowledge. In a parallel manner, he emphasized the role of ritual in treatment, providing by catharsis.
The first hospital wards for the mentally disturbed opened from the 8th century in the Middle East, notably at Baghdad Hospital under Rhazes, with the first dedicated asylums opening from the 15th Century in Egypt, Spain and then the rest of Europe, notoriously at Bedlam in England.
In the 16th century, Johann Weyer argued that some cases of alleged witchcraft were actually psychiatric symptoms, as others had argued before him. Different categories of mental health conditions became systematically considered by physicians in the context of neurology, a term coined in the 17th century from the work of Thomas Willis. In 1758, William Battie gave impetus to the study and treatment of mental disturbance as a medical speciality. From the late 18th Century, the moral treatment movement sought to make asylums more humane and therapeutic as well as custodial, an approach developed partly from the work of physicians, notably Philippe Pinel, who also developed new ways of categorizing mental health conditions.
Psychiatry developed as a clinical and academic profession in the early 19th Century, particularly in Germany. The field sought to systematically apply concepts and tools from general medicine and neurology to the study and treatment of abnormal mental distress and disorder. The term psychiatry was coined in 1808 by Johann Christian Reil, from the Greek “psyche” (soul) and “iatros” (doctor). Official teaching first began in Leipzig in 1811, with the first psychiatric department established in Berlin in 1865. Benjamin Rush pioneered the approach in the United States. The American Psychiatric Association was founded in 1844. Psychiatric nursing developed as a profession.
Early in the 20th Century, neurologist Sigmund Freud developed the field of psychoanalysis and Carl Jung popularized related ideas. Meanwhile Emil Kraepelin developed the foundations of the modern psychiatric classification and diagnosis of mental health conditions. Others who notably developed this approach included Karl Jaspers, Eugen Bleuler, Kurt Schneider and Karl Leonhard. Adolf Meyer was an influential figure in the first half of the twentieth century, combining biological and psychological approaches.
Sigmund Freud
Psychoanalysis did not originate in academic psychology, which was focused in university laboratories and was concerned with normal psychology and topics like perception, sensation, etc. On the contrary psychoanalysis is focused on abnormal behavior and treatment. In addition, it is more focused on the unconscious than the conscious. Yet it shares a basic background with Behavioralism and Functionalism in that it is mechanistic and evolutionary in nature.
Hypnosis played a role in the development of psychoanalysis. Although Franz Anton Mesmer (1734-1815) developed mesmerism or animal magnetism, James Braid (1795-1860) legitimized the scientific study of hypnosis. Jean Martin Charcot (1825-1893) used hypnosis to treat hysteria as a neurologist. Pierre Janet (1859-1947), Charcot’s student, further emphasized the psychic nature of hysteria via the role of fixed ideas, impaired memory, and unconscious forces.
In accord with the development and application of hypnosis, the discussion of unconscious mental phenomena was popular in both public and scientific circles in the late 1800s. The existence of the unconscious was well recognized but no one had a clear means of studying it. Also catharsis was a well recognized and frequently discussed topic in German intellectual circles.
Jean Martin Charcot (1825-1893)
Charcot saw hysteria as due to faulty heredity, which when combined with a traumatic event (subjectively determined) and the emotions generated in the trauma, produced somatic manifestations. Yet Charcot’s examination of the patient was essentially neurological, looking for hysterical stigmata-zones of anesthesia and hysterogenous zones-that could trigger an attack. Charcot further postulated a link between the ideas and emotions involved in the trauma and the subsequent symptoms, but this was not delineated. Charcot’s most important contribution was the recreation or demonstration of hysterical symptoms through hypnosis in susceptible people. Hypnosis was seen as heightened suggestibility, suggesting that there is a range of phenomena between the normal, the hypnotic and the hysterical. Thus ideas and emotions triggered by trauma are separated from associations and are placed in a different state (the unconscious), later emerging in a weakened state of consciousness. Thus emotions and ideas could be transformed into symptoms. Although Janet and Charcot did not know why this occurred, its recognition was an important step. Up to this time the emphasis in psychiatry was in the demarcation of syndromes, based on the delineation of differences in symptoms.
Psychiatry was used by some totalitarian regimes as part of a system to enforce political control, for example in Nazi Germany, the Soviet Union under Psikhushka, and the apartheid system in South Africa. For many years during the mid-20th century, Freudian and neo-Freudian thinking dominated psychiatric thinking. Social Psychiatry developed.
From the 1930s, a number of treatment practices came in to widespread use in psychiatry, including inducing seizures (by ECT, insulin or other drugs) or cutting connections between parts of the brain (leucotomy or lobotomy). In the 1950s and 1960s, lithium carbonate, chlorpromazine and other typical antipsychotics and early antidepressant and anxiolytic medications were discovered, and psychiatric medication came in to widespread use by psychiatrists and general physicians.
Coming to the fore in the 1960s, the field attracted an anti-psychiatry movement challenging its theoretical, clinical and legal legitimacy. Psychiatrists notably associated with critical challenges to mainstream psychiatry included R.D. Laing and Thomas Szasz.
Along with the development of fields such as genetics and tools such as neuroimaging, psychiatry moved away from psychoanalysis back to a focus on physical medicine and neurology and to search for the causes of mental health conditions within the genome and the neurochemistry of the brain. Social psychiatry became marginalised relative to biopsychiatry. “Neo-Kraepelinian” categories were codified in diagnostic manuals, notably the ICD and DSM, which became widely adopted. Robert Spitzer was notable in this development. New drugs came in to common use, notably SSRI antidepressants and atypical antipsychotics.
Psychiatry was involved in the development of psychotherapies. Neo-Freudian ideas continued, but there was a trend away from long-term psychoanalysis to more cost-effective or evidence-based approaches, particularly cognitive therapy from the work of Aaron Beck. Other mental health professions, particularly clinical psychology, were becoming more established and competing with or working with psychiatry.
During the last third the 20th century, the institutional confinement of people diagnosed with symptoms of mental health conditions steadily declined, particularly in more developed countries. Among the reasons for this trend of deinstitutionalization were pressure for more humane care and greater social inclusion, advances in psychopharmacology, increases in public financial assistance for people with disabilities, and the Consumer/Survivor Movement. Developments in community services followed, for example psychiatric rehabilitation and Assertive Community Treatment.
It has been argued that different methods of historical analysis, for example focusing on individual/technical achievements or focusing on social factors and social constructs, can lead to different histories of psychiatry.
The Latest Diagnostic and Statistical Manual of Mental Disorders from the American Psychiatric Association.
Two main classifications of mental health conditions are in use today. The ICD-10 (International Classification of Diseases) is produced and published by the World Health Organisation and includes a section on psychiatric conditions, and is used to some extent worldwide. The Diagnostic and Statistical Manual of Mental Disorders (DSM), produced and published by the American Psychiatric Association, is solely focused on mental health conditions and is the main classification tool in the United States. It is currently in its fourth revised edition (IV-TR, published 2000) and is also used world-wide, perhaps more so than the ICD-10. The ICD-10 and the DSM are considered roughly on a par with one another, and an explicit concern in the development of the DSM-IV was compatibility with the diagnostic categories and codes of the ICD. The lack of a case example version of the ICD-10 is considered a problem by some[citatioeeded]. The Chinese Society of Psychiatry has also produced a diagnostic manual, the Chinese Classification of Mental Disorders (CCMD).
The stated intention of diagnostic manuals is typically to develop replicable and clinically useful categories and criteria, to facilitate consensus and agreed standards, whilst being atheoretical as regards etiology. However, the categories are nevertheless based on particular psychiatric theories and data; they are broad and often specified by numerous possible combinations of symptoms, and many of the categories overlap in symptomology or typically occur together. While originally intended only as a guide for experienced clinicians trained in its use, the nomenclature is now widely used by clinicians, administrators and insurance companies in many countries.
The DSM has five axes:
Axis I: Psychiatric disorders
Axis II: Personality disorders / mental retardation
Axis III: General medical conditions
Axis IV: Social functioning and impact of symptoms
Axis V: Global Assessment of Functioning (described using a scale from 1 to 100)
Common axis I disorders between the two systems include substance dependence and abuse (e.g. alcohol dependence); mood disorders (e.g. depression, bipolar disorder); psychotic disorders (e.g. schizophrenia, schizoaffective disorder); and anxiety disorders (e.g. post-traumatic stress disorder, obsessive-compulsive disorder). Axis II disorders include borderline personality disorder, schizotypal personality disorder, avoidant personality disorder and antisocial personality disorder.
SENSATION – the process by which information about the world is registered by the senses and transmitted to the brain
PERCEPTION, according to a generally acceptable definition, is the process of organizing and interpreting sensory data by combining them with the results of previous experience. We can also say that perception is the mental representation (reflexion) of an object as a whole, whereas sensations represent separate properties of the object (its colour, shape, sound, etc.). This definition indicates that perception is a complex process involving the past as well as the present and involving an external stimulus as well as an internal response. Isolated properties of objects never influence us separately from each other, thus, in psychology we usually speak of perception and not of sensations.
Neurophysiology of perception.
The intactness of the sense organs and tracts is a necessary precondition for accurate perception. For example, colour blindness interferes with the perception of color. However, the perception of physical stimuli involves more than simply the sensory pathways specific to a particular modality of stimulation. Recent work has placed considerable emphasis on the role of the reticular formation in the perception of stimuli. This activating system is apparently essential to arousal, which must precede the reception of a stimulus from any modality.
INDIVIDUAL DEVELOPMENT AND EXPERIENCE.
One tends to perceive the more important stimuli rather than the less important. Since the attribute of importance is based on individual experience and interests, two people in the same situation may perceive very different things, and yet both may be accurate. What each perceives is a function of his own learning and experience. For example, the letter A would be simply a collection of lines to someone who does not know how to read.
An experience that predisposes an individual to certain types of perceptions is called a set. The more ambiguous the stimulus, the more its perception is determined by the set or proclivities of the subject. And the stronger the set of the individual, the more it determines his perception. The meaning attributed to a particular stimulus by an individual is a function of the ambiguity of the stimulus and the strength of his set.
The quantities disorders of perceptions:
1) hyperesthesia; 2) hypoesthesia; c) anesthesia
The quality disorders of perceptions:
1) illusions; (physical, physiological, psychological-affective and pareydolias);
2) hallucinations (Auditory Hallucinations, Visual Hallucinations, Tactile, or Haptic, Hallucinations, Olfactory Hallucinations, Gustatory Hallucinations);
3) psychosensor disorders
HALLUCINATIONS
Hallucinations may occur in each of the five sensory modalities: patients may hear, see, feel, smell, or taste things that are not in fact there.
Patients react differently to these experiences. Occasionally patients have insight about these and recognize that although these experiences appear as vivid and clear as things that other people hear and see, they are not in fact real. More often, however, patients insist these experiences are real, and when the physician denies hearing or seeing the same things, the patients may assume that the physician is lying or is perhaps part of the plot against them. In such cases trying to convince patients that they are wrong is useless. One patient hallucinated the devil sitting in another chair in the room; the physician, trying to convince the patient otherwise, got up and sat in the chair the devil was supposed to be in. The patient was unimpressed and commented that “everyone knows the devil is a spirit.”
Hallucinations, like delusions, may or may not be mood-congruent. For example, a voice announcing a guilty verdict and a death sentence would be quite congruent with the mood of a profoundly depressed patient who had a delusion of sin. Or an exalted manic patient might well see angels descending and hear a chorus of heavenly voices from the clouds. An example of a mood-incongruent hallucination, however, is found in a depressed patient who heard giggling voices uttering obscenities. Although exceptions do exist, in general the finding of mood incongruent hallucinations argues strongly against the diagnosis of a mood disorder, suggesting rather a diagnosis of schizophrenia, schizoaf-fective disorder, or some other similar condition.
Hallucinations may also be seen in dementia, delirium, secondary psychosis, alcohol hallucinosis, various intoxications, and in some withdrawal states.
Auditory Hallucinations
At times only simple sounds are heard: bells, cracklings, “the voice of chewing,” or the roar of animals. Music may be heard. When voices occur they may be only in a whisper or mumbled indistinctly. At other times they may be distinct, even overpowering. Short phrases or just single words may be heard: “whore,” “murderer,” “guilty,” “look-out.” At other times patients hear long sentences, even conversations.
For the most part what the voices say is unpleasant, even frightening. Sometimes, however, patients hear soothing voices, even congratulatory ones.
At times patients hear “command hallucinations,” or voices that direct them to do specific things. They may be innocuous: a voice commanding them to get dressed or to not eat certain foods. At other times, however, patients may be commanded to do dangerous things: the voices may even tell them to kill themselves or someone else. Most often patients are able to resist such command hallucinations, but not always.
Most patients have a sense of where the voices come from. They may be “in the air,” in walls or furniture, or emanating from television, radios, or electrical appliances. Not uncommonly they are heard in the midst of music, in what is said on the radio, in rushing water, or from the wind as it rustles the leaves of trees. At times they are located in the body, perhaps the spleen, or some other organ.
Kurt Schneider
Kurt Schneider identified three types of auditory hallucinations that he believed were of the “first rank” and found more commonly in schizophrenia than in other conditions. These three hallucinations consist of the following: voices talking to each other, voices commenting on what the patient is doing, and voices that repeat or speak out loud the patient’s thoughts. This last hallucination, often
known as “audible thoughts,” is perhaps the most suggestive of schizophrenia. Patients hear their own thoughts spoken out loud, as if they were echoed, and they often believe that others can hear them also and thus know what the patients are thinking. Sometimes, indeed, they feel as if the thoughts were spoken from a loudspeaker.
Musical Hallucinations fall under the category of auditory hallucinations and describe a disorder in which a sound is perceived as instrumental music, sounds, or songs. It is a very rare disorder, reporting only 0.16% in a cohort study of 3,678 individuals.[1]
Early Cases
According to Oliver Sacks’ Hallucinations, the first known medical report of musical hallucinations was published in 1846, by French alienist Jules Baillarger.[2] However, the first scientific description of the disorder was reported in the early 1900s. In the last two decades, Berrios has reported case studies in 1990 and 1991 along with Keshavan et al. in 1992. Berrios concluded that confirmed diagnoses of deafness, ear disease, brain disease, advanced age and drug use are all important factors in the development of musical hallucinations. After analyzing 46 cases, Berrios found a female predominance of 80% in women over the age of 60. The study concluded that musical hallucinations were more likely to be seen in elderly women affected by deafness or brain disease than in individuals with no psychiatric illness at all.[3][4]
Keshevan and Berrios were the first authors to identify classes of musical hallucinations. These classes consisted of hearing loss, coarse brain disease (i.e. tumors), epileptic disorder, stroke, and psychiatric disorder. Although no statistical analyses were performed, the authors stated that deafness was the most strongly related factor in musical hallucinations and that there was a female predominance, which could entail a genetic component.[1][3][4]
Description of Disorder
As technology has developed, we have been able to gain a better understanding of the specific contents within a musical hallucination. In 73 individual cases reviewed by Evers and Ellger, 57 patients heard tunes that were familiar, while 5 heard unfamiliar tunes. These tunes ranged from religious pieces to childhood favorites, and also included popular songs from the radio. Vocal and instrumental forms of classical music were also identified in some patients. Keshavan found that the consistent feature of musical hallucinations was that it represented a personal memory trace. Memory traces refer to anything that may seem familiar to the patient, which indicated why certain childhood or familiar songs were heard.[1][4]
Functional Imaging
Positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) show that musical hallucinations activate a wide variety of areas in the brain including the following: auditory areas, motor cortex, visual areas, basal ganglia, brainstem, pons, tegmentum, cerebellum, hippocampi, amygdala, and peripheral auditory system.[2]
Causes
Investigators have successfully narrowed down the major factors that are associated with musical hallucinations. Evers & Ellgers compiled a significant portion of musical hallucination articles, case studies etc. and were able to categorize five major etiologies:
· Psychiatric Disorders
· Focal Brain Lesion
· Epilepsy
G2. Visual Hallucinations
Visual hallucinations may range in complexity from simple flashes of light to the most detailed scenes. Sometimes shadows are seen “out of the corner of the eye.” At other times fleeting shapes are seen in the darkness of the night, “as if someone were there.’ Colored shapes may float in the air. The faces of others may become disfigured, grotesque, or even melt. Bodies may float through the air; a skeleton is seen outside the window. The heavenly host appears on the horizon; the jurors march in to render their verdict.
Visual hallucinations that accompany auditory ones have no special diagnostic significance and may be seen in schizophrenia, mania, depression, dementia, delirium, and in other disorders. However, when visual hallucinations occur in the complete absence of auditory ones, then one is most likely dealing with a dementia, delirium, or secondary psychosis.
Tactile, or Haptic, Hallucinations
Any imaginable tactile sensation may be hallucinated. In formication, bugs may be felt crawling over the face or swarming over the body. Internal stirrings or electric sensations deep in the bowels may be felt. Burns or prickings of hundreds of needles are felt on the skin. Less commonly, tactile hallucinations may be pleasant, often sexual in nature: a feeling as of soft velvet drawn across the skin, ineffable pleasures are felt, and at times orgasm may occur.
Tactile hallucinations may occur in schizophrenia, mania, depression, intoxications (especially with cocaine), and withdrawal from alcohol or sedative-hypnotics.
Olfactory Hallucinations
Patients may speak of a foul stench, “as if death.” Poisonous gas may be smelled, or sulfurous fumes “from hell.” Occasionally there may be pleasant odors, as of perfume. Such hallucinations may be seen in schizophrenia and also in simple or complex partial seizures, so-called “uncinate fits.”
Gustatory Hallucinations
Hallucinated tastes are almost always disagreeable. Food may taste rotten or putrid. Patients may experience a taste of feces.
Metallic tastes may be found in simple or complex partial seizures and may also occur in some poisonings with heavy metals.
“Hallucinations” in healthy people
It is important to note that similar phenomena may be experienced in the absence of mental disorder. These experiences have been recorded over thousands of years. In the Judeo-Christian records, God spoke to Adam on the sixth day, giving him instructions about how to behave in the Garden of Eden (Genesis, 2:16 -17). God spoke to Moses from a burning bush, and on another occasion, He dictated the Ten Commandments (Exodus, 34:27).
In the Islamic records, the Angel Gabriel spo ke to Mohammed on many occasions. On the first occasion he said, “Oh, Mohammed, of a verity thou art the prophet of God”. On subsequent occasions, over many years, the angel spoke the entire Koran to him.
Voices of secular origin have also been experienced by many prominent people. Sigmund Freud, the father of psychoanalysis wrote, “During the days when I was living alone in a foreign city….I quite often heard my name suddenly called by an unmistakable and beloved voice….” The hearing of a family member’s voice when separated from them is not uncommon among recently bereaved people and those lost in the wilderness. In such circumstances being alone and wishing to be with loved individuals appears to have greater explanatory power than supernatural factors and mental disorders.
Mahatma Gandhi, the man who almost single handedly achieved Indian independence from Britain, relied on an “inner voice” for guidance. Toward the end of his life the voice said, “You are on the right track, move neither to your left, nor right, but keep to the Pridmore S. Download of Psychiatry, Chapter 5. Last modified: March 2007 2 straight and narrow.” Others of great resolve have described similar “inner voices”, which have helped with determination and goal achievement. Healthy, average individuals may hear voices which are not of spiritual or pathological origin. Professor Henry Sidgewick conducted the “International Census of Waking Hallucinations in the Sane”, in the 1890s. Seventeen thousand people from England, Russia and Brazil were surveyed. Nearly 10% r eported they had experienced an unexplained perception; 2.9% of the total reported having heard a voice. A century later Professor Allen Tien conducted a study of 15 000 members of the general population in the USA and found that 2.3% had heard voices (Tien A, 1991). In a number of careful studies of small populations of university students the experience of hearing voices has been reported by a much higher p roportion of subjects.
Thus, healthy people may, from time to time, hear voices. Care has been takein these paragraphs to avoid calling these experiences, hallucinations, even though these experiences satisfy the technical definition.
Briefly, there are differences between the voices heard by healthy individuals and the hallucinations of those with mental disorders. In healthy individuals, the voice is usually as if from one person, speaking comprehensibly, in a helpful and comforting manner.
Auditory hallucinations in mental disorders, in contrast, often involve more than one voice, sometimes arguing, sometimes commenting about the patient, frequently making little sense, often in a threatening and frightening manner.
ILLUSIONS are perceptions that are associated with an outside stimulus, but the stimulus is wrongly interpreted. For example, lapping water may be heard as laughter. T echnically, these are not hallucinations, as they are associated with a stimulus. Illusions are frequently visual, and they are usually the result of a medical condition. The condition which most commonly causes illusions is delirium tremens (DTs), the disturbed state which can complicate alcohol withdrawal. Objects such as creases in bed covers may be perceived as snakes, insects or other animals. Folk law says that people in DTs see pink elephants. In clinical practice, however, small organisms are more commonly “seen”.
Fig. The Ponzo illusion may help you understand the moon illusion. Picture the two white bars as resting on the railroad tracks. In the drawing, the upper bar is the same length as the lower bar. However, because the upper bar appears to be farther away than the lower bar, we perceive it as longer. The same logic applies to the moon illusion.
Fig. Some interesting perceptual illusions. Illusions are a normal part of perception.
Other perceptual difficulties include heightened and changed perceptions. By heightened perceptions is meant sounds seem unnaturally clear, loud or intense, colours appear more brilliant or beautiful, or details of the environment seem to stand out in a particularly interesting way. By changed per ceptions is meant changes are perceived in the shape or size of people and inanimate objects in the environment. Changes may continue while the patient watches. These phenomena may occur in psychotic disorders; on occasions psychotic patients may be difficult to engage in conversation because they are concentrating on continuously changing perceptions. Patients may spend long periods looking in a mirror, watching their own face change. Heightened and changed perceptions may occur in other disorders, including the non-psychotic, anxiety disorders.
A pseudohallucination is an involuntary sensory experience vivid enough to be regarded as a hallucination, but recognised by the patient not to be the result of external stimuli. In other words, it is a hallucination that is recognized as a hallucination, as opposed to a “normal” hallucination which would be perceived as real. An example used in psychiatry is the hearing of voices which are “inside the head” according to the patient; in contrast, a hallucination would be indistinguishable to the patient from a real external stimulus, e.g. “people were talking about me”.
The term is not widely used in the psychiatric and medical fields, as it is considered ambiguous; the term nonpsychotic hallucination is preferred. Pseudohallucinations, then, are more likely to happen with a hallucinogenic drug.
A further distinction is sometimes made between pseudohallucinations and parahallucinations, the latter being a result of damage to the peripheral nervous system.
They are considered a feature of conversion disorder, somatization disorder, and dissociative disorders. Also, pseudohallucinations can occur in people with visual loss, with the typical such type being Charles Bonnet syndrome.
Pseudohallucinations can happen between dream and reality.
Closed-eye hallucinations and closed-eye visualizations (CEV) are a distinct class of hallucination. These types of hallucinations generally only occur when one’s eyes are closed or when one is in a darkened room. They are a form of phosphene. Certain users report closed-eye hallucinations under the influence of psychedelics. These are reportedly of a different nature than the “open-eye” hallucinations of the same compounds. Closed eye hallucination is directly related to a chronic type. Levels of CEV perception
There are five known levels of CEV perception which can be achieved either through chemical stimuli or through meditative relaxation techniques. Level 1 and 2 are very common, and often happen every day. It is still normal to experience level 3, and even level 4, but only a small percentage of the population do this without psychedelic drugs, meditation or extensive visualization training.
Level 1: Visual noise
CEV noise simulation
The most basic form of CEV perception that can be immediately experienced iormal waking consciousness involves a seemingly random noise of pointillistic light/dark regions with no apparent shape or order.
This can be seen when the eyes are closed and looking at the back of the eyelids. In a bright room, a dark red can be seen, owing to a small amount of light penetrating the eyelids and taking on the color of the blood within them. In a dark room, blackness can be seen or the object can be more colourful. But in either case it is not a flat unchanging redness/blackness. Instead, if actively observed for a few minutes, one becomes aware of an apparent disorganized motion, a random field of lightness/darkness that overlays the redness/blackness of your closed eyelids.
For a person who tries to actively observe this closed-eye perception on a regular basis, there comes a point where if he or she looks at a flat-shaded object with his or her eyes wide open, and tries to actively look for this visual noise, he or she will become aware of it and see the random pointillistic disorganized motion as if it were a translucent overlay on top of what is actually being seen by his or her open eyes.
When seen overlaid onto the physical world, this CEV noise does not obscure physical vision at all, and in fact is hard to notice if the visual field is highly patterned, complex, or in motion. When active observation is stopped, it is not obvious or noticeable, and seemingly disappears from normal physical perception. Individuals suffering from visual snow see similar noise but experience difficulty blocking it from conscious perception.
The noise probably originates from thermal noise exciting the photoreceptor cells in the retina; compare Eigengrau.
Level 2: Light/dark flashes
Some mental control can be exerted over these closed-eye visualizations, but it usually requires a bit of relaxation and concentration to achieve. When properly relaxed it is possible to cause regions of intense black, bright white or even colors such as yellow, green, or pink to appear in the noise. These regions can span the entire visual field, but seem to be fleeting iature.
Level 3: Patterns, motion, and color
CEV pattern simulation. Note that this can be quite different from real life experience
This level is relatively easily accessible to people who use LSD, and appears to be what most people refer to as colourful visuals.
However, it is also accessible to people involved in deep concentration for long. When lying down at night and closing the eyes, right before sleep the complex motion of these patterns can become directly visible without any great effort thanks to hypnagogic hallucination. The patterns themselves might resemble fractals.
Level 4: Objects and things
This is a fairly deep state. At this level, thoughts visually manifest as objects or environments. When this level is reached, the CEV noise seems to calm down and fade away, leaving behind an intense flat ordered blackness. The visual field becomes a sort of active space. A side component of this is the ability to feel motion when the eyes are closed.
Some paranormal researchers believe that remote places can be viewed in this state and have named it remote viewing.
Opening the eyes returns one to the normal physical world, but still with the CEV object field overlaid onto it and present. In this state it is possible to see things that appear to be physical objects in the open-eye physical world, but that aren’t really there.
Level 5: Overriding physical perception
If inducing by drugs or mental disease, this is the point where it appears to the outside world that a person is either unconscious or insane. The internal CEV perceptions and think-it/feel-it perceptions become stronger than physical perceptions, and completely override and replace open-eye physical perceptions. This can be a potentially dangerous state if a person is still mobile while in a different imagined world, but by this time most people are motionless and not likely to do something hazardous to themselves or others.[5] This is the point where most hallucinogenic references say it is a good idea to have a “sitter” present to watch over the person using the chemicals, and keep them from accidentally harming themselves or others while deep into their own world.
This level can be entered from complete sensory deprivation, as experienced in an isolation tank, but even there it requires great relaxation.
According to lucid dreaming researcher Stephen LaBerge, perceptions can come from either the senses or imagination. A inhibitory system involving in the thalamus, likely involving serotonergic neurons, inhibits imaginary perceptions from becoming too activated so they turn into hallucinations. This system is inhibited during REM sleep, and the imagination can freely run into the perceptual systems. What happens at level 5 is likely that this system is inhibited, just like in REM sleep, by different causes like sensory deprivation, psychedelic drugs or meditative relaxation techniques.
What is not a CEV
Image burn-in (afterimage)
Image burn-in occurs when very bright objects lie in one’s field of vision, and should not be confused with closed-eye hallucinations. Visual burn-in from bright lights is visible for a few minutes after closing the eyes, or by blinking repeatedly, but the burn-in effect slowly fades away as the retina recovers, whereas the waking-consciousness CEV noise will not disappear if observed continuously over a period of time.
Corneal liquid
CEV does not involve the liquid and air bubbles on the surface of the cornea, which can also be seen by extremely nearsighted people when looking at bright point-light sources with glasses/contacts removed. Also called “Floaters” – often appear as cells floating across the eye. Half-closing and reopening the eyelids creates a very definite wiper-ridge in the corneal liquid that is readily visible. Fully closing and reopening the eyelids also stirs up the corneal liquid which settles down after a brief moment. The motion of waking-consciousness CEV noise is not so directly and physically controllable and repeatable. This is not necessarily only associated with extreme nearsightedness.
Blue-sky sprites
CEV does not seem to be related to the “sprites” (blue field entoptic phenomenon) that can be seen as dots darting around when staring up into a bright blue sky on a sunny day (not looking at the sun). These dots superimposed over a flat blue background are white blood cells moving through the blood vessels of the retina. The motion of waking-consciousness CEV noise is uniformly random compared to the waking-consciousness blue-sky sprite motion.
Physical retinal stimulation
CEV is unrelated to the visual noise seen when the retina is physically stimulated. The retina can be made to produce light patterns of visual noise simply by one rubbing their eyes somewhat forcefully in a manner that increases intraocular pressure. Additionally retinal noise can be produced by touching near the rear of the eyeball (for example, if one closes their eyes, looks all the way left, and lightly touches the rightmost part of the eye socket, this produces visual noise in the shape of a circle that appears at the left side of the visual field – a practice that is neither painful nor dangerous). None of these are closed-eye hallucinations.
MEMORY is an ability to revive past sensory impressions, experiences, and learned ideas.
Memory includes three basic mental processes:
1) registration – the ability to perceive, recognize and establish
information in the central nervous system; it is also called fixation;
2) retention – the ability to retain registered information; and
3) recall – the ability to retrieve stored information at will.
Long-term memory
Memory disorders and aging
Normal aging, although not responsible for causing memory disorders, is associated with a decline in cognitive and neural systems including memory (long-term and working memory). Many factors such as genetics and neural degeneration have a part in causing memory disorders. In order to diagnose Alzheimer’s disease and dementia early, researchers are trying to find biological markers that can predict these diseases in younger adults. One such marker is a beta-amyloid deposit which is a protein that deposits on the brain as we age. Although 20-33% of healthy elderly adults have these deposits, they are increased in elderly with diagnosed Alzheimer’s disease and dementia.
Additionally, traumatic brain injury, TBI, is increasingly being linked as a factor in early-onset Alzheimer’s disease.
One study examined dementia severity in elderly schizophrenic patients diagnosed with Alzheimer’s disease and dementia versus elderly schizophrenic patients without any neurodegenerative disorders. In most cases, if schizophrenia is diagnosed, Alzheimer’s disease or some form of dementia in varying levels of severity is also diagnosed. It was found that increased hippocampal neurofibrillary tangles and higher neuritic plaque density (in the superior temporal gyrus, orbitofrontal gyrus, and the inferior parietal cortex) were associated with increased severity of dementia. Along with these biological factors, when the patient also had the apolipoprotein E (ApoE4) allele (a known genetic risk factor for Alzheimer’s disease), the neuritic plaques increased although the hippocampal neurofibrillary tangles did not. It showed an increased genetic susceptibility to more severe dementia with Alzheimer’s disease than without the genetic marker.
As seen in the examples above, although memory does degenerate with age, it is not always classified as a memory disorder. The difference in memory betweeormal aging and a memory disorder is the amount of beta-amyloid deposits, hippocampal neurofibrillary tangles, or neuritic plaques in the cortex. If there is an increased amount, memory connections become blocked, memory functions decrease much more than what is normal for that age and a memory disorder is diagnosed.
The cholinergic hypothesis of geriatric memory dysfunction is an older hypothesis that was considered before beta-amyloid deposits, neurofibrillary tangles, or neuritic plaques. It states that by blocking the cholinergic mechanisms in control subjects you can examine the relationship between cholinergic dysfunction and normal aging and memory disorders because this system when dysfunctional creates memory deficits.
Memory disorders can range from mild to severe, but they all result from some kind of neurological damage to the structures of the brain, thus hindering the storage, retention and recollection of memories.
Memory disorders can be progressive, like Alzheimer’s or Huntington’s disease, or immediate, like those resulting from traumatic head injury. Most disorders are exacerbated by the effects of ageing, which remains the single greatest risk factor for neurodegenerative diseases in general.
Research and analysis of individual case studies of memory disorders have yielded many important insights into how human memory works, although much more work remains to be done. In recent years, neuro-imaging techniques such as MRI, CAT and PET scans have also aided in the analysis of how memory disorders affect the brain physiologically and neurologically.
Disorders of memory
AMNESIA
Amnesia is the general term for a condition in which memory (either stored memories or the process of committing something to memory) is disturbed or lost, to a greater extent than simple everyday forgetting or absent-mindedness. Amnesia may result either from organic or neurological causes (damage to the brain through physical injury, neurological disease or the use of certain drugs), or from functional or psychogenic causes (psychological factors, such as mental disorder, post-traumatic stress or psychological defence mechanisms).
There are two main types of amnesia: anterograde amnesia (where the ability to memorize new things is impaired or lost because data does not transfer successfully from the conscious short-term memory into permanent long-term memory); and retrograde amnesia (where a person’s pre-existing memories are lost to conscious recollection, beyond an ordinary degree of forgetfulness, even though they may be able to memorize new things that occur after the onset of amnesia). Anterograde amnesia is the more common of the two. Sometimes both these types of amnesia may occur together, sometimes called total or global amnesia. Another type of amnesia is post-traumatic amnesia, a state of confusion and memory loss that occurs after a traumatic brain injury. Amnesia which occurs due to psychological factors is usually referred to as psychogenic amnesia.
Many kinds of amnesia are associated with damage to the hippocampus and related areas of the brain which are used in the encoding, storage and retrieval of memories. If there is a blockage in the pathways along which information travels during the processes of memory encoding or retrieval, or if whole regions of the brain are missing or damaged, then the brain may not be able to form new memories or retrieve some old ones.
The usual causes of amnesia are lesions to the brain from an accident or neurological disease, but intense stress, alcohol abuse, loss of oxygen or blood flow to the brain, etc, can all also cause amnesia, as sometimes can treatments such as electro-convulsive therapy. For example, intense stress can cause the sympathetic nervous system to activate the adrenal glands, which then secrete certain hormones into the bloodstream which can significantly affect the plasticity of the brain’s neurons (i.e. their ability to change and strengthen connections), especially those in the hippocampus.
In most cases, amnesia is a temporary condition, lasting from a few seconds to a few hours, but the duration can be longer depending on the severity of the disease or trauma, up to a few weeks or even months. Although it is very rare for anyone to experience total (permanent) amnesia, one well-known case of long-lasting and acute total (retrograde and anterograde) amnesia, perhaps the worst case of amnesia ever recorded, is that of the British musician Clive Wearing, who suffered damage to his brain as a result of an encephalitis virus in 1985. Because the damage was to an area of his brain required to transfer memories from working memory to long-term memory, he is completely unable to form lasting new long-term memories, and his memory is therefore limited to a short-term memory of between 7 and 30 seconds, to the extent that he will greet his wife like a long-lost friend even if she only left to go into the kitchen 30 seconds ago. However, Wearing still recalls how to play the piano and conduct a choir, despite having no recollection of having received a musical education, because his procedural memory was not damaged by the virus.
In general, memories of habits (procedural memory) are usually better preserved than memories of facts and events (declarative memory), and the most distant long-term memories, such as those of childhood, are more likely to be preserved. When memories return, older memories are usually recalled first, and then more recent memories, until almost all memory is recovered.
Retrograde amnesia is a form of amnesia where someone is unable to recall events that occurred before the development of the amnesia, even though they may be able to encode and memorize new things that occur after the onset.
Retrograde amnesia usually follows damage to areas of the brain other than the hippocampus (the part of the brain involved in encoding new memories), because already exisiting long-term memories are stored in the neurons and synapses of various different brain regions. For example, damage to Broca’s or Wernicke’s areas of the brain, which are specifically linked to speech production and language information, would probably cause language-related memory loss. It usually results from damage to the brain regions most closely associated with declarative (and particularly episodic) memory, such as the temporal lobe and prefrontal cortex. The damage may result from a cranial trauma (a blow to the head), a cerebrovascular accident or stroke (a burst artery in the brain), a tumour (if it presses against part of the brain), hypoxia (lack of oxygen in the brain), certain kinds of encephalitis, chronic alcoholism, etc.
Typically, episodic memory is more severely affected than semantic memory, so that the patient may remember words and general knowledge (such as who their country’s leader is, how everyday objects work, colours, etc) but not specific events in their lives. Procedural memories (memory of skills, habits and how to perform everyday fucntions) are typically not affected at all.
Retrograde amnesia is often temporally graded, meaning that remote memories are more easily accessible than events occurring just prior to the trauma (sometimes known as Ribot’s Law after the 19th Century psychologist Thйodule-Armand Ribot), and the events nearest in time to the event that caused the memory loss may never be recovered. This is because the neural pathways of newer memories are not as strong as older ones that have been strengthened by years of retrieval and re-consolidation. While there is no actual cure for retrograde amnesia, “jogging” the victim’s memory by exposing them to significant articles from their past will often speed the rate of recall.
Anterograde amnesia is the loss of the ability to create new memories, leading to a partial or complete inability to recall the recent past, even though long-term memories from before the event which caused the amnesia remain intact. Sufferers may therefore repeat comments or questions several times, for example, or fail to recognize people they met just minutes before.
Anterograde amnesia may be drug-induced (several benzodiazepines are known to have powerful amnesic effects, and alcohol intoxication also has a similar effect) or it follows a traumatic brain injury or surgery in which there is damage to the hippocampus or medial temporal lobe of the brain, or an acute event such as a concussion, a heart attack, oxygen deprivation or an epileptic attack. Less commonly, it can also be caused by shock or an emotional disorder.
Research shows that anterograde amnesia results from a failure of memory encoding and storage. New information is processed normally, but almost immediately forgotten, never making it into the regions of the brain where long-term memories are stored. More specifically, iormal use, neurons in the mammillary bodies of the hypothalamus make connections with the thalamus, which in turn makes connections with the cortex of the brain, where long-term memories are stored. Anterograde amnesia can therefore result from damage to the hypothalamus and thalamus and the surrounding cortical structures, so that encoded memories are never stored since connections between hippocampus and cortex are disrupted.
Usually, sufferers from anterograde amnesia lose declarative memory (the recollection of facts), but they retaion-declarative, or procedural, memory (the learning of skills and habits). For instance, they may be able to remember or learn how to do things, such as talking on the phone or riding a bicycle, but they may not remember what they had eaten for lunch earlier that day. This is because procedural memory does not rely on the hippocampus and medial temporal lobe memory system in the same way as declarative memory. There have, however, been cases where anterograde amnesia patients lose only the episodic part of their declarative memory (that part which relates to autobiographical information with a temporal and/or spatial context), and not the semantic part (factual information, such as language, history, geography, etc, with autobiographical association).
When there is damage to just one side of the medial temporal lobe, the neuroplasticity of the brain (its ability to re-map its neural connections wheecessary) can often allow the opportunity for normal, or near-normal, functioning for memories with time.
Psychogenic amnesia, also known as functional amnesia or dissociative amnesia, is a disorder characterized by abnormal memory functioning in the absence of structural brain damage or a known neurobiological cause. It results from the effects of severe stress or psychological trauma on the brain, rather than from any physical or physiological cause. It is often considered to be equivalent to the clinical condition known as repressed memory syndrome.
There are two main types of psychogenic amnesia: global amnesia and situation-specific amnesia. Global amnesia, also known as fugue state, refers to a sudden loss of personal identity lasting a few hours or days, often accompanied by severe stress or depression and often involving extended periods of wandering and confusion. It is very rare, and usually resolves over time (although memory of the fugue episode itself may remain lost), often helped by therapy. Situation-specific amnesia is a type of psychogenic amnesia that occurs as a result of a severely stressful event, as part of post-traumatic stress disorder.
Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after exposure to any event that results in psychological trauma, which manifests itself in constant re-experiencing of the original trauma through flashbacks or nightmares and avoidance of any stimuli associated with the trauma, as well as increased arousal (such as difficulty falling or staying asleep, anger and hypervigilance).
It is most commonly associated with traumatic events or violent experiences involving emotional shock, such as being mugged or raped or involved in car crash. Those at increased risk include those sexually or physically abused during childhood, those who have experienced domestic violence, natural disasters, terrorist acts, etc, soldiers who have experienced combat, and essentially anyone who has experienced any sufficiently severe psychological stress, internal conflict or intolerable life situation.
Freudian psychology suggests that psychogenic amnesia is an act of self-preservation, where the alternative might be overwhelming anxiety or even suicide. Unpleasant, unwanted or psychologically dangerous memories are repressed or blocked from entering the consciousness as a kind of subconscious self-censorship, but they remain in the unconscious. Neurologically, normal autobiographical memory processing is blocked by an imbalance of stress hormones such as glucocorticoids and mineralocorticoids in the brain, particularly in the regions of the limbic system involved in memory processing.
Such repressed memories may be recovered spontaneously, years or decades after the event, triggered by a particular smell, taste or other identifier. Because it is due to psychological rather than physiological causes, psychogenic amnesia can also sometimes be helped by therapy. Repressed memories may be accessed by psychotherapy, hypnotism or other techniques, although it is often difficult to distinguish a true repressed memory from a false one without corroborating evidence.
Those who suffer from psychogenic amnesia tend to lose their biographical or episodic memories, (to the extent of not even being able to remember their owames and addresses), particularly of the events leading up to the trigger event, but usually preserve their semantic and procedural memories, and the ability to create new memories. Episodes of psychogenic amnesia can last from a few hours to several days, or sometimes even months, although severe cases are very rare. Because it is due to psychological rather than physiological causes, it can sometimes be helped by therapy.
The constant remembering and re-imagining of traumatic events causes them to be reinforced and re-consolidated time after time, and the memory is so strong and realistic that it is encoded almost as a new current event each time, rather than as an old memory. Thus, the memories need to be “re-filed” in their proper place (in the past), and recent advances in the understanding of neuroplasticity (the brain‘s ability to rewire and reconfigure itself) have led to some promising treatments. One example is the use of beta blockers, such as propanolol, while repeatedly reading a detailed account of the traumatic event, thus chemically blocking neurons so that, over time, the account becomes just another story without the old traumatic personal associations.
Confabulation is a memory disturbance characterized by information that appears to be made up rather than true. Confabulation is distinguished from lying as there is no intent to deceive and the person is unaware the information is false. Although individuals can present blatantly false information, confabulation can also seem to be coherent, internally consistent, and relatively normal. Individuals who confabulate present incorrect memories ranging from “subtle alternations to bizarre fabrications”, and are generally very confident about their recollections, despite contradictory evidence. Most known causes of confabulation are caused by brain damage or dementias, such as alcoholism, aneurysm or Alzheimer’s disease.
Two distinct types of confabulation are often distinguished: spontaneous and provoked.
Spontaneous, or primary, confabulations do not occur in response to a cue and seem to be involuntary. Spontaneous confabulation is relatively rare, may result from the interaction between frontal lobe pathology and organic amnesia, and is more common in cases of dementia.
Provoked, momentary, or secondary, confabulation represents a normal response to a faulty memory and is common in both amnesia and dementia. Provoked confabulations can become apparent during memory tests. Another distinction found in confabulations is that between verbal and behavioral. Verbal confabulations are spoken false memories and are more common, while behavioral confabulations occur when an individual acts on their false memories.[6] Confabulated memories of all types most often occur in autobiographical memory, and are indicative of a complicated and intricate process that can be led astray at any point during encoding, storage, or recall of a memory.[4] This type of confabulation is commonly seen in Korsakoff’s syndrome.
A blackout is a phenomenon caused by the intake of an alcoholic beverage or other substance in which long term memory creation is impaired or there is a complete inability to recall the past. Blackouts are frequently described as having effects similar to that of anterograde amnesia, in which the subject cannot recall any events after the event that caused amnesia. ‘Blacking out’ is not to be confused with the mutually exclusive act of ‘passing out‘, which means loss of consciousness. Research on alcohol blackouts was begun by E. M. Jellinek in the 1940s. Using data from a survey of Alcoholics Anonymous (AA) members, he came to believe that blackouts would be a good determinant of alcoholism. However, there are conflicting views as to whether this is true. The negative psychological effects of an alcohol-related blackout are often worsened by those who suffer from anxiety disorders.
Fragmentation of memory is a memory disorder, in which patient is unable to organize memories in space or/and time. The impaired person can remember things, but cannot pinpoint when the events happened, and has poor sense of time – personal timeline is distorted, months, or even years are confused even for relatively recent events.
The impaired person usually suffers from physical damage or underdevelopment of hippocampus. It may be a genetic disorder, or consequence of some traumatic disorder, like PTSD. [1] Dysfunctional brain often has other related consequences, like oversensitivity to some stimuli, impulsiveness, lack of direction in life, sometimes aggressiveness and distorted perception of self and ability to truly empathize with others, which is usually masked on the first sight.
Many times there is a link between dissociative disorders and memory fragmentation. Two common dissociative disorders in which fragmentation of memory caormally be found are: Dissociative Amnesia – Not to be confused with general amnesia where the sufferer is unable to recall whole periods of time as short as a couple weeks or months all the way up to years, dissociative amnesia is much more common than the general type of the disorder. With the dissociative version of the disorder there is a failure to recall specific events, normally events that were accompanied by some sort of trauma. The disorder also branches out into the emotional state of the mind upon experiencing trauma. [4] Meaning that at times the person will be able to remember the specifics of the events (date, time, location, people involved etc.) but the strong emotional ties to the experience is what becomes fragmented in the creation of the memory. Dissociative Fugue – This disorder normally revolves around a specific trip taken by the person suffering from the disorder. They can travel great distances and not remember the trip. These unremembered trips are normally the result of the individual trying to escape an unbearable situation and many times while traveling the person unknowingly suffers some degree of identity distortion or at times assuming a completely new identity. One of the unique characteristics of this disorder is that upon completing the trip the individual normally remembers the trip and all the details associated with it but while the events are happening there is no recollection of time passing or where they physically are.
Korsakoff’s syndrome (also called Korsakoff’s dementia, Korsakoff’s psychosis, or amnesic-confabulatory syndrome) is a neurological disorder caused by a lack of thiamine (vitamin B1) in the brain. Its onset is linked to chronic alcohol abuse and/or severe malnutrition. The syndrome is named after Sergei Korsakoff, a Russian neuropsychiatrist who described it during the late 19th century.
Acute Korsakoff-Like Amnestic Syndrome Resulting from Left Thalamic Infarction Following a Right Hippocampal Hemorrhage
There are six major symptoms of Korsakoff’s syndrome:
2. retrograde amnesia, severe memory loss
3. confabulation, that is, invented memories which are then taken as true due to gaps in memory sometimes associated with blackouts
4. meager content in conversation
5. lack of insight
6. apathy – the patients lose interest in things quickly and generally appear indifferent to change.
These symptoms are caused by a deficiency of thiamine (vitamin B1), which is thought to cause damage to the medial thalamus and mammillary bodies of the hypothalamus as well as generalized cerebral atrophy. These brain regions are all parts of the limbic system, which is heavily in involved in emotion and memory.
When Wernicke’s encephalopathy accompanies Korsakoff’s syndrome, the combination is called the Wernicke-Korsakoff syndrome. Korsakoff’s is a continuum of Wernicke’s encephalopathy, though a recognised episode of Wernicke’s is not always obvious.
Korsakoff’s involves neuronal loss, that is, damage to neurons; gliosis which is a result of damage to supporting cells of the central nervous system; and hemorrhage or bleeding in mammillary bodies. Damage to the dorsomedial nucleus or anterior group of the thalamus (limbic-specific nuclei) is also associated with this disorder. Cortical dysfunction may have arisen from thiamine deficiency, alcohol neurotoxicity, and/ or structural damage in the diencephalon.
Originally it was thought that a lack of initiative and a flat affect were important characteristics of emotion. Studies have questioned this, proposing that it is not necessarily a symptom of Korsakoff’s. Research suggesting that Korsakoff patients are emotionally unimpaired has made this a controversial topic. It can be argued that apathy, which usually characterizes Korsakoff patients, reflects a deficit of emotional expressions, without affecting the experience or perception of emotion.
Korsakoff’s Syndrome causes deficits in declarative memory in most patients, but keeps implicit spatial, verbal, and procedural memory functioning intact.
Research has also suggested that Korsakoff patients have impaired executive functions, which can lead to behavioral problems and interfere with daily activities. It is unclear however, which executive functions are affected most.
At first it was thought that Korsakoff patients used confabulation to fill in memory gaps. However, it has been found that confabulation and amnesia do not necessarily co-occur. Studies have shown that there is dissociation between provoked confabulation, spontaneous confabulation (which is unprovoked) and false memories. That is, patients could be led to believe certain things that haven’t happened, just like people without Korsakoff’s syndrome.
Signs include:
· Apathy
· Ataxia
· Coma
· Paralysis of muscles controlling the eye
· Retrograde and anterograde amnesia
· Tremor
· Anosognosia – Lack of insight to or awareness of the condition
Post-hypnotic amnesia is the inability in hypnotic subjects to recall events that took place while under hypnosis. This can be achieved by giving individuals a suggestion during hypnosis to forget certain material that they have learned either before or during hypnosis. Individuals who are experiencing post-hypnotic amnesia cannot have their memories recovered once put back under hypnosis and is therefore not state dependent. Nevertheless, memories may return when presented with a pre-arranged cue. This makes post-hypnotic amnesia similar to functional amnesia as it disrupts the retrieval process of memory. It has been suggested that inconsistencies in methodologies used to study post-hypnotic amnesia cause varying results.
Categories of post-hypnotic amnesia
Spontaneous and suggested post-hypnotic amnesia can occur or be induced in an individual.
Spontaneous post-hypnotic amnesia
For most of the 19th century, investigators reported that post-hypnotic amnesia only occurred spontaneously as scientific knowledge regarding this form of amnesia was minimal. Spontaneous post-hypnotic amnesia represents a slight memory impairment that results as a consequence of being put under hypnosis or being tested. This form of amnesia can also be experienced across susceptibility groups, but to a much lesser extent and magnitude to suggested post-hypnotic amnesia.
Spontaneous amnesia has also been difficult to determine as research bias has been found to influence in many cases. In one study participants were put into two groups; one was to receive amnesic instructions and half were not given the instructions. The next day the groups were reversed. Results showed that there was little spontaneous amnesia across all participants, leading to doubts towards the actual occurrence of amnesia. It was later found that those more susceptible to hypnosis were more susceptible to suggested post-hypnotic amnesia and not spontaneous amnesia. These results suggest that spontaneous amnesia is less common than suggested amnesia and that when high results of spontaneous amnesia are recorded, some incidences may be false.
Suggested post-hypnotic amnesia
Suggested post-hypnotic amnesia involves the suggestion to hypnotized persons that following hypnosis they will be unable to accurately recall specific material (e.g. stimuli or events learned while under hypnosis) until they receive a reversibility cue. This type of post-hypnotic amnesia is the most commonly used within research surrounding post-hypnotic amnesia due it’s controlled nature.
Suggested amnesia has been found to result in a more significant memory loss than spontaneous amnesia, regardless of the order of induction. On average, more individuals experience suggested amnesia and there appears to be a moderate effect across individuals of all levels of hypnotic susceptibility. Suggested post-hypnotic amnesia also involves a “temporary, retrieval-based dissociation between episodic and semantic memory”. However, it is more common for highly hypnotizable individuals to remember less information than low hypnotizable individuals or controls while under suggested post-hypnotic amnesia.
Post-hypnotic amnesia is reversible, a characteristic that distinguishes it from other forms of amnesia that arise primarily from traumatic brain injury. Whereas the retrieval of memories under retrograde amnesia is a slow and labour-intensive process, the reversal of hypnotically-induced amnesia can occur with a simple suggestion or reversal cue (e.g., “when I clap my hands, you will remember everything”).
Types of post-hypnotic amnesia
Recall amnesia
Post-hypnotic recall amnesia refers to an individual’s inability to recall, when in a normal conscious state, the events that occurred during hypnosis. Evidence for this type of post-hypnotic amnesia is seen in a typical research model testing where nonsense syllables, that were paired during hypnosis, are unable to be recalled post hypnotically when a suggestion for amnesia was given during hypnosis. Recall amnesia for word associations tend to be very high when done by post-hypnotic individuals, with some studies showing one hundred percent total recall amnesia. This amnesia can also be measured by asking individuals, after their hypnosis has been terminated, to describe what they have been doing since they first laid down on the couch for their hypnosis session. When using this method for experimental testing, the hypnosis session will typically involve several tests or activities that the subject will engage in. Recall amnesia can then be measured by the amount of accurate tasks and activities the subject is able to remember.
Recognition amnesia
Recognition amnesia equates to an impairment of an individual’s Recognition memory brought on by amnesia. As event-related potentials have been found to be sensitive to familiar stimuli in the absence of recognition impairments it has been suggested that individuals who report amnesia after hypnosis might not be experiencing post-amnesia recognition impairments. Instead, they may not be accurately describing their experience and confuse having amnesia for a lack of attention during encoding of tested stimuli.[13]
Source amnesia
Post-hypnotic source amnesia refers to the ability of individuals to correctly recall information learned during hypnosis without the recollection of where the information was acquired. In a typical study examining this type of amnesia, individuals are administered a hypnotic induction procedure which is immediately followed by a series of questions concerning unfamiliar facts, for example “what year was Freud born in?”. Subjects who are unable to correctly answer these questions are informed of the correct answers. These individuals are then administered a suggestion to be amnesic for everything that occurred during the period of which they are hypnotized. After the hypnotic session, those who exhibit post-hypnotic source amnesia, when asked the same unfamiliar questions again, will respond with the correct answers but will not be able to state where they learned the answer, or, more commonly, rationalize an incorrect source of their answer.
Childhood amnesia,
also called infantile amnesia, is the inability of adults to retrieve episodic memories before the age of 2–4 years, as well as the period before age 10 of which adults retain fewer memories than might otherwise be expected given the passage of time. For the first 1–2 years of life, brain structures such as the limbic system, which holds the hippocampus and the amygdala and is involved in memory storage, are not yet fully developed. Research has demonstrated that children can remember events from before the age of 3–4 years, but that these memories decline as children get older.
Research has shown that children have the capacity to remember events that happened to them from age 1 and before, but as they get older they tend to be unable to recall memories from their youngest years. When the offset of childhood amnesia is defined as the age of first memory, then offset occurs around 3.5 years[7] though it can range from 2 to 5 years, depending on the memory retrieval method[8] and age of the respondent. However, when the offset of childhood amnesia is defined as the age at which the majority of memories are personal recollections rather than known events, then offset occurs at approximately 4.5 years old. This may be due to children’s development of understanding and knowledge of their own memory.
Changes in encoding, storage and retrieval of memories during early childhood are all important when considering childhood amnesia.[10] Research shows differences between gender and culture, which is implicated in the development of language. Childhood amnesia is particularly important to consider in regard to false memories and the development of the brain in early years. Proposed explanations of childhood amnesia are Freud’s Trauma theory, neurological development, development of the cognitive self, emotion and language.
Prosopamnesia presents itself in patients as an inability to recognize people they have previously encountered based on their faces. In this way, it is very easily mistaken as prosopagnosia, which is an inability to perceive or recognize faces. Prosopagnosia is a deficit that occurs earlier in the neural circuit while the facial stimuli is being processed, whereas prosopamnesia takes effect when the brain attempts to encode the processed facial stimuli into memory. Because the distinction between prosopamnesia and prosopagnosia is so close in the neurological circuit, the only phenotypic difference between the two is in the breadth of faces to which a patients symptoms apply. Prosopagnosics cannot recognize faces, even of people within their own families over the span of a lifetime. Prosopamnesiacs show a memory for facial stimuli that they learned prior to the onset of their condition (in the case of acquired prosopamnesia) or for facial stimuli that they have encountered repeatedly for long periods of time (in the case of congenital prosopamnesia).
There are currently only two diagnosed cases of prosopamnesia. This is likely due to the fact that it can easily be misdiagnosed as prosopagnosia based on symptoms. Some doctors have even recognized distinctions in deficits of facial perception and facial memory encoding and classified them as subfamilies of prosopagnosia.[1] This lack of consistency within the scientific community for classifying patients with facial memory encoding deficits is one reason that prosopamnesia has such rare diagnosis. Most of the current knowledge about how prosopamnesia works within the brain is hypothesized, but not proven, due to lack of case studies. As doctors become aware of the distinction between prosopagnosia and prosopamnesia, proper and more frequent diagnosis of prosopamnesia may occur.
Individuals with hyperthymesia can recall almost every day of their lives iear perfect detail, as well as public events that hold some personal significance to them. Those affected describe their memories as uncontrollable associations, when they encounter a date, they “see” a vivid depiction of that day in their heads.[4] Recollection occurs without hesitation or conscious effort.
It is important to draw a distinction between those with hyperthymesia and those with other forms of exceptional memory, who generally use mnemonic or similar rehearsal strategies to memorise long strings of subjective information. Memories recalled by hyperthymestic individuals tend to be personal, autobiographical accounts of both significant and mundane events in their lives. This extensive and highly unusual memory does not derive from the use of mnemonic strategies; it is encoded involuntarily and retrieved automatically. Despite being able to remember the day of the week on which a particular date fell, hyperthymestics are not calendrical calculators like some people with autism or savant syndrome. Rather, hyperthymestic recall tends to be constrained to a person’s lifetime and is believed to be an unconscious process.
Although hyperthymestics are not autistic, and likewise savants do not memorise autobiographical information, there are certain similarities between the two conditions. Like autistic savants, individuals with hyperthymesia have an unusual and obsessive interest in dates. Russian psychologist Aleksandr Luria documented the famous case of mnemonist Solomon Shereshevskii, who was quite different from the first documented hyperthymestic known as AJ in that he could memorise virtually unlimited amounts of information deliberately, while AJ could not – she could only remember autobiographical information (and events she had personally seen on the news or read about). In fact, she was not very good at memorising anything at all, according to the study published in ‘’Neurocase’’. Hyperthymestic individuals appear to have poorer than average memory for arbitrary information. Another striking parallel drawn between the two cases was that Shereshevskii exemplified an interesting case of synaesthesia and it has been suggested that superior autobiographical memory is intimately tied to time-space synaesthesia.
Cases
By 2006 twenty cases of hyperthymesia had been confirmed, the most famous of these being AJ (who later revealed her identity as school administrator Jill Price). Her case was originally reported by researchers from the University of California, Irvine, Elizabeth Parker, Larry Cahill and James McGaugh, and is credited as being the first case of hyperthymesia. AJ can apparently recall every day of her life from when she was 14 years old: “Starting on February 5th, 1980, I remember everything. That was a Tuesday.”
In March 2009 Price was interviewed for an article in Wired magazine by Gary Marcus, a cognitive psychologist at New York University. Price’s brain had been subject to a brain scan and the hippocampus and prefrontal cortex had been reportedly normal. Marcus claimed, however, that her brain resembled “those of people with obsessive-compulsive disorder” and suggested that her remarkable memory might be “the byproduct of obsession”, claiming also that “the memory woman clings tightly to her past”. Price has since reacted angrily to such claims and McGaugh has also expressed skepticism for such an explanation. In September 2012 Price gave her first interview in over a year for the UK’s Channel 4 documentary The Boy Who Can’t Forget and provided an insight into just how difficult life can be for people who have this ability.
As the condition has become better known, more and more people claiming to have hyperthymestic abilities have emerged. In the aftermath of the 2006 Neurocase publication alone, more than 200 people contacted McGaugh; however only a handful of cases were determined to be actual cases of hyperthymesia. The second verified case was Brad Williams, the third was Rick Baron, and in 2009 Bob Petrella became the fourth person diagnosed with hyperthymestic syndrome. All three men are left-handed.
On December 19, 2010, actress Marilu Henner was featured on the US television program 60 Minutes for her superior autobiographical memory ability. Henner claimed she could remember almost every day of her life since she was 11 years old. The show was initially pitched as a story featuring hyperthymestic violinist Louise Owen, but the reporter Lesley Stahl volunteered her friend Henner as having a similar ability.
In June 2012 the case of “HK” was reported, a blind 20-year old man who could clearly recall every day of his life since the age of about 11. He told researchers that his memories are rich in sensory and emotional details, regardless of whether they are from years ago or yesterday. Ninety percent of his memories are in the first person, compared with an average of 66 percent in the general population. Brandon Ally and his team, at Vanderbilt University, Nashville, Tennessee, conducted a series of tests with the subject, including a brain scan which was compared with 30 age-matched controls. His brain was smaller than average (probably a result of his premature birth at 27 weeks). His right amygdala, however, was 20 percent larger and there was enhanced functional connectivity between the right amygdala and hippocampus and in other regions.
In September 2012 UK’s Channel 4 screened the documentary The Boy Who Can’t Forget, which examined the memory of 20 year-old Aurelien Hayman from Cardiff, a student at Durham University, who remembers practically every day of his life from the age of 10. Hayman is the first Briton to be identified as possessing this ability, and he views it positively. When Hayman’s brain was scanned by a team led by Professor Giuliana Mazzoni at the University of Hull, whilst he was prompted to remember a series of dates, a series of “visual areas” of the brain were activated, with much greater speed than would be expected iormal brain function. Potential problems with total recall were illustrated. The documentary also featured 62 year-old TV producer Bob Petrella whose memory has allowed him to catalogue the events from his “favourite days” over many years into an extensive scrapbook.
A 25-year-old Global Marketing Specialist from Turkey was the last case encountered. M.A.‘s extraordinary ability to remember almost everything that she had experienced shocked the scientists. She put her experience of Hyperthymesia in these words: “I did not realize this until a co-worker of mine told me that I remember everything in details and he was suspicious if it was a psychological disorder. When I went to see an expert about my case, this expert told me that it was highly possible that Hyperthymesia was my case. He also mentioned that that was nothing to worry about, which was a big relief.”
Investigation of memory
Memory is a very broad function which includes several distinct abilities, all of which can be selectively impaired and require individual testing. There is disagreement as to the number of memory systems, depending on the psychological perspective taken. From a clinical perspective, a view of five distinct types of memory, is in most cases sufficient. Semantic memory and episodic memory (collectively called declarative memory or explicit memory); procedural memory and priming or perceptual learning (collectively called non-declarative memory or implicit memory) all four of which are long term memory systems; and working memory or short term memory. Semantic memory is memory for facts, episodic memory is autobiographical memory, procedural memory is memory for the performance of skills, priming is memory facilitated by prior exposure to a stimulus and working memory is a form or short term memory for information manipulation.
· California Verbal Learning Test
· Cambridge Prospective Memory Test (CAMPROMPT)
· Memory Assessment Scales (MAS)
· Rey Auditory Verbal Learning Test
· Rivermead Behavioural Memory Test
· Test of Memory and Learning (TOMAL)
· Test of Memory Malingering (TOMM)
MMSE
A nurse, physician, physician assistant, or mental health worker will ask a number of questions. The test can be done in the home, in an office, nursing home, or hospital. Sometimes, a psychologist with special training will do more extensive tests.
The most common test used is called the mini-mental state examination (MMSE) or Folstein test.
The following may be tested:
APPEARANCE
The health care provider will check your physical appearance, including:
· Age
· Dress
· General level of comfort
· Gender
· Grooming
· Height/weight
ORIENTATION
The health care provider will ask questions such as:
· What is your name?
· How old are you?
· Where do you work?
· Where do you live?
· What day and time is it?
· What season is it?
ATTENTION SPAN
Attention span may be tested earlier, because this fundamental skill can influence the rest of the tests.
The provider will want to test:
· Your ability to complete a thought
· Your ability to think and problem solve
· Whether you are easily distracted
You may be asked to do the following:
· Start at a certaiumber, and then begin to subtract backwards by 7s.
· Spell a word such as “WORLD” forward, and then backward.
· Repeat up to 7 numbers forward, and up to 5 numbers in reverse order.
RECENT AND PAST MEMORY
The provider will ask questions related to recent people, places, and events in your life or in the world.
Three items may be presented, and the person may then be asked to repeat them, and then recall them after 5 minutes.
The provider will ask about your childhood, school, or events that occurred earlier in life.
LANGUAGE FUNCTION
The provider will point to everyday items in the room and ask you to name them, and possibly to name less common items.
You may be asked to say as many words as possible that start with a certain letter, or that are part of a certain category, in 1 minute.
You may be asked to read or write a sentence.
JUDGMENT
This part of the test looks at your ability to solve a problem or situation. You may be asked:
· “If you found a driver’s license on the ground, what would you do?”
· “If a police officer approached you from behind in a car with lights flashing, what would you do?”
