How would you argue that a poem is the perfect form of expression?

In my opinion, poetry's main competition as a form of expression is prose.  

Because prose is your main competition, you are going to need to focus on the negatives of prose and focus on the positives of poetry.  With that said though, do not completely ignore the positive things that prose does.  If you begin your essay by saying that prose is horrible, you risk alienating your reader.  You do not wanta reader...

In my opinion, poetry's main competition as a form of expression is prose.  

Because prose is your main competition, you are going to need to focus on the negatives of prose and focus on the positives of poetry.  With that said though, do not completely ignore the positive things that prose does.  If you begin your essay by saying that prose is horrible, you risk alienating your reader.  You do not want a reader on the defensive.  Start with a thesis statement that admits the positives of prose while stating that poetry is superior.  For example: "Although prose is a solid form of expression, poetry is a far superior form of written expression."  

The above thesis is specific in its intent, but it is broad enough to allow the body of your essay to pick and choose aspects of prose and poetry while still supporting your thesis statement.    

While I do enjoy reading prose more than poetry, I will admit that poetry does certain things better.  Focus on poetry's ability to create vivid imagery in a relatively short amount of space.  Poetry is typically very image dense when compared with the number of words on a page.  Prose on the other hand often takes multiple pages to explain a similar image.  I would also focus on poetry's ability to create rhythm while incorporating rhyme.  Prose can be detailed for sure, but it just can't ever create that "sing song" feel.  If the goal of expression is to tap into an emotional core, poetry taps the core more quickly than prose. That's why people write poems and set them to music. They are called songs.  Nobody puts prose to music.  

I would also make sure that the positives that you choose to mention regarding prose are also positives that poetry can do as well, only better. Your job isn't to discredit prose.  Your job is to show poetry as superior.  Take character development for example. Prose is often praised for its ability to concretely develop a character in deep ways. Poetry is capable of doing that too.  In fact, that's what the dramatic monologue poem style is all about.  My favorite in that genre is Browning's "My Last Duchess." The character of the Duke is so well created in that poem.

For your conclusion, try to push your reader into further considering and exploring poetry as a superior form of expression.  

What are sense organs? |

Structure and Functions

The sense organs of the body include the cutaneous sense organs, the organs of chemical reception, the organs of vision or sight, and the organs of hearing and balance. The skin is the major organ of sensation for touch, pressure, cold, warmth, and pain; the nasal epithelium and taste buds are the major organs of chemoreception; the eyes are the major organs of vision or sight; and the ears are the major organs of both hearing and balance.

There are five types of cutaneous receptors within the skin, each with a different type of sensory nerve ending and each with a different spatial pattern of distribution. Free (naked) nerve endings are sensitive to pain and are widely distributed over the body’s skin surface, especially at the base of each hair. Overstimulation of any type of nerve ending also results in a sensation of pain, but these nerve endings are so exposed that any stimulation at all is felt as an overstimulation. All the remaining cutaneous receptors are encapsulated in one of several types of end organs. Of these, the end bulbs of Krause may be temperature sensitive; they are most numerous around the conjunctiva of the eye and along the glans of the penis and the glans of the clitoris.

The Pacinian corpuscles each contain a single central nerve fiber, enclosed in many concentric layers of semitransparent tissue resembling the bulb of an onion. These structures, which are about one to four millimeters in diameter, are sensitive to deep pressure and are distributed throughout the skin, principally within the dermal papillae. They are most numerous on the palm of the hand, the sole of the foot, and the insides of many joints such as the front of the elbow or the back of the knee. The tactile (Meissner’s) corpuscles each consist of an oval, bulblike swelling in which the nerve endings run around in spiral patterns at right angles to the long axis. Meissner’s corpuscles are sensitive to light touch and are most numerous along the fingertips (and the hand in general), the tongue and lips, parts of the eye, and the skin of the mammary nipple or papilla. The corpuscles of Ruffini are enclosed in connective tissue sheaths perpendicular to the nerve that serves them. The axons of this nerve branch repeatedly within the corpuscle and these branches intertwine, each ending in a tiny knob. Corpuscles of Ruffini are sensitive to warmth and are very numerous over the fingertips, the forearm, and the skin of the face. The evidence to associate particular nerve endings with particular sensations (such as the Meissner’s corpuscles with light touch) comes largely from patterns of spatial distribution: the areas of the body most sensitive to touch are also those with the highest densities of Meissner’s corpuscles.

Neuromuscular spindles occur in most voluntary muscles and are sensitive to the state of contraction or relaxation of the muscle fibers. The spindle consists of a muscle fiber or small bundle of such fibers, around which are wrapped several turns of infrequently branching sensory nerve endings. The tendons of many muscles also frequently contain neurotendinous spindles, encapsulated structures in which a bundle of tendon fibers receive branched nerve endings. These nerve endings branch slightly just before reaching the tendon fibers but then lose their sheaths and branch profusely within the tendon. These neurotendinous spindles act as stretch receptors, sensitive to the state of stretching of the tendon.

Chemoreceptors of the body include those tissues sensitive to certain chemicals. The carotid body, a swelling within the carotid artery of the neck, contains tissue sensitive to the carbon dioxide or acid content of the blood; it stimulates the breathing reflex when the carbon dioxide level is too high. The taste buds of the tongue are sensitive to the taste of a variety of chemical substances present in moderate concentrations. Each taste bud contains gustatory cells along with nonsensitive supporting (sustentacular) cells. Experimental evidence points to five basic types of taste sensations: sweet (like sugar), bitter (like quinine), sour (like vinegar or citric acid), salty (like sodium chloride), and savory (like chicken broth). Sensitivity to each of these four basic tastes has its own characteristic pattern of distribution over the tongue and palate.

The nasal epithelium is responsible for olfaction, or smell, which is a sensitivity to chemical substances in much smaller concentrations. Most of the nasal epithelium is associated with the nose and the nasal passages, but a small part of this epithelium has become attached instead to the roof of the mouth, where it forms the vomeronasal (or Jacobson’s) organ, which “smells” the contents of the mouth (mostly food). The nasal epithelium is structurally unusual in that the cell bodies of the sensory cells originate within the epithelium and their nerve endings (axons) migrate inwardly to the brain, through the cribriform plate, forming the first cranial nerve or olfactory nerve. All other sensory nerves in the body grow outward from the central nervous system, and their cell bodies are located where their growth began.

Attempts have been made to classify smells according to a scheme similar to the classification system used for tastes, but there are many more basic smells than there are tastes—lists vary from six to twenty to more than ninety—and there is no general agreement on any of these schemes.

The eyes are the body’s principal visual receptors. (Some evidence also exists of the brain’s own ability to sense daily changes in the level of light intensity, especially in the pineal body.) The primary parts of the eye include the eyelids, cornea, lens, ciliary body, iris diaphragm, pupil, aqueous humor, vitreous humor, retina, choroid coat, scleroid coat, and optic nerve. The eyelids protect the front of the eye and prevent injury to the eye by closing. The cornea is the transparent covering of the front of the eye; the lens is the transparent, almost spherical body that focuses rays of incoming light onto the retina; and the ciliary body is a largely connective tissue structure (also containing some muscle tissue) that supports the lens. The colored part of the ciliary body is the iris diaphragm; muscle fibers within the iris diaphragm adjust the size of the pupil for different brightness levels of light. The opening in the middle of the iris diaphragm is called the "pupil." The aqueous humor is the watery fluid in front of the lens, while the vitreous humor is the thick, jellylike fluid behind the lens.

The light-sensitive portion of the eye is the retina. It is almost spherical in shape and consists of two layers: a sensory layer on the inside (closer to the front) and a pigment layer surrounding and behind the sensory layer. Within the sensory layer are contained both the rods, which are sensitive to finer details, and the cones, which are sensitive to colors. The eye’s most sensitive area is called the "area centralis"; it is centered upon a depression called the "fovea." The choroid coat is the connective tissue layer immediately surrounding the retina, which is continuous with the pia mater that surrounds the brain. The scleroid coat is the stronger connective tissue layer that surrounds the choroid coat; it is continuous with the dura mater surrounding the brain. The optic nerve fibers originate from the sensory layer of the retina, where they converge toward a spot called the "blind spot," marking the place where the nerve fibers turn inward toward the brain. A majority of the optic nerve fibers cross over to the opposite side of the brain via the optic chiasma, but a small proportion of the fibers remains on the same side without crossing over. Experiments on the physiology of vision have led researchers to conclude that there are three separate types of color receptors (cones) in the retina, sensitive principally to red, green, and blue regions of the spectrum. All other color sensations can be simulated experimentally in people with normal vision by a suitable combination of red, green, and blue stimuli.

The ears are special sense organs devoted to the two distinct functions of hearing and balance. The ear may be divided anatomically into outer, middle, and inner portions or functionally into a cochlear portion for hearing and a vestibular portion for balance. The outer (external) ear consists of a flap called the "pinna" (or "external ear flap") and a tubelike cavity called the "external acoustic meatus." Within the external ear, sound impulses exist as waves of compressed or decompressed (rarefied) air, forming a series of longitudinal waves that vibrate in the same direction in which they are transmitted. The tympanic membrane
(eardrum) is a vibrating membrane that marks the boundary between the outer and middle ears.

The middle ear consists of a cavity containing three tiny bones, the auditory ossicles. Within the middle ear, the vibrations of the tympanic membrane set up a series of vibrations within these tiny bones. The three auditory ossicles are called the "malleus" (hammer), "incus" (anvil), and "stapes" (stirrup). The malleus gets its name from its hammerlike shape, which includes a long handle (manubrium) extending across the tympanic membrane. The incus, the second of the auditory ossicles, rests against the malleus at one end and the stapes at the other. The stapes is shaped like a stirrup, in which the foot is placed when riding a horse. The flat base of the stapes is called the "footplate," in analogy to the corresponding part of a stirrup; this footplate rests against the fenestra ovalis of the inner ear. The opening in the stapes is penetrated by an artery called the "stapedial artery." The cavity of the middle ear connects to the pharynx by means of a tube, the pharyngotympanic or Eustachian tube.

The inner ear is entirely housed within the petrosal bone. It can be divided into cochlear (hearing) and vestibular (balance) portions. The cochlear portion of the inner ear begins with two windows, the fenestra ovalis (oval window) and fenestra rotundum (round window), communicating between the middle ear and the inner ear. Behind the fenestra ovalis lies a vestibule, filled with a fluid called "perilymph" and extending into a long scala vestibuli. Behind the fenestra rotundum lies another long tube, the scala tympani, also filled with perilymph and running parallel to the scala vestibuli. Between these two tubes lies a third, the scala media or cochlear duct, filled with a different fluid called "endolymph." Together, the three are prolonged into a spiral coil called the "cochlea" (Latin for “snail”), which has a bit more than three complete turns. At the end of this coil, the scala media ends, and the scala vestibuli and scala tympani join with one another by means of an intervening loop called the "helicotrema." The basilar membrane separates the scala tympani and the cochlear duct. The spiral organ (organ of Corti) runs within the cochlear duct along the basilar membrane, not far beneath a tectorial membrane that is suspended within the cochlear duct.

The outer ear receives vibrations that travel through the air and transmits these vibrations to the tympanic membrane. In the middle ear, the vibrations of the tympanic membrane are transmitted through the malleus, incus, and stapes to the oval window. These vibrations are transmitted through the perilymph of the inner ear (vestibular portion), where they cause vibrations of the basilar membrane. The vibrating basilar membrane causes vibrations within the endolymph and also in the tectorial membrane, but the tectorial membrane is less flexible than the basilar membrane, creating regions of greater and lesser pressure within the endolymph. The hair cells of the spiral organ are sensitive to these pressure differences and send out nerve impulses to the brain, where they are interpreted as sounds.

The vestibular portion of the inner ear includes two interconnected chambers called the "sacculus" and the "utriculus," both filled with endolymph. The sacculus has a downward extension called the "lagena," and it also connects into the scala media of the cochlear portion of the ear. From the utriculus emerge three semicircular ducts, approximately at right angles to one another, all filled with endolymph: an anterior vertical duct, a posterior vertical duct, and a horizontal duct. Each semicircular duct runs through a bony semicircular canal, filled with perilymph. Each duct has a bulblike swelling, the ampulla, at one end. Each ampulla has a patch, or macula, of sensory structures called "neuromasts," which are sensitive to movements in fluids such as endolymph. Other maculae, or patches of neuromasts, are located in the sacculus, the utriculus, and the lagena.

The vestibular portion of the inner ear is sensitive to movements and especially to acceleration. Normally, this acceleration is caused by gravity, but nonlinear movements (such as the swerving of a fast-moving vehicle around a curve) may also result in accelerations that cause fluid movements within the semicircular canals. These movements are perceived by the sensitive hair cells (neuromasts) within each ampulla. Spinning around or other sudden acceleration causes temporary dizziness (vertigo) and a consequent loss of balance.

Disorders and Diseases

Several types of medical specialists deal with problems of the various sense organs: ophthalmologists deal with diseases of the eye; otorhinolaryngologists deal with diseases of the ears (oto-), nose (rhino-), and throat (larynx); and neurologists deal with all the senses. All these specialists first conduct diagnostic tests in order to detect any sensory malfunction and to determine the probable cause; they then provide whatever treatment may be available for each condition.

The ability to distinguish tastes diminishes gradually with age in older persons as the number of gustatory cells declines, but complete loss of taste is rare. Persons with diminished taste are at greater risk for accidental poisoning and malnutrition. Except for the decline of taste among the elderly, other defects of smell or taste are relatively uncommon and may be indicative of more serious neurological problems such as brain damage or nerve damage or endocrine problems such as Kallman syndrome. The inability to smell is a rare condition known as "anosmia." Similarly, loss of cutaneous sensations, even over a small portion of the body, is usually indicative of nerve damage, while diminished sensitivity to touch stimuli is a common aspect of aging. Such impairment can lead to injuries, pressure ulcers, and temperature-related problems such as heat stroke.

Disorders of the eye range from easily correctable vision problems to total blindness. Impaired function of one or more of the three types of color receptors results in one of the several types of color blindness. The most common type, red-green color blindness, is inherited as a sex-linked recessive trait and is thus more common in men than in women. Blindness may result from various defects or injuries: a defective lens or cornea may limit vision to large objects, and a defective retina may limit perception to light and darkness only. Total blindness results if the optic nerve is damaged or missing. More common visual defects include myopia(nearsightedness), hyperopia (farsightedness), and astigmatism (differences in vision along different axes), all of which can be corrected with glasses or contact lenses or by surgical procedures. A failure of the mechanism that drains fluid from the interior of the eyeball may result in a buildup of ocular pressure, a condition known as "glaucoma." In times past, when treatment for glaucoma was not readily available, most cases resulted in permanent blindness. Glaucoma can now be treated, however, either surgically or with drugs. Several changes occur to the lens of the eye in older individuals. As the lens becomes more rigid with advancing age, reading and other near-vision tasks become more difficult, a condition known as "presbyopia." Also frequent among older people are cataracts, tiny opaque grains that cloud up the lens and reduce the ability to see clearly. Untreated cataracts may eventually result in blindness, but various forms of treatment are available to prevent this from occurring.

Diseases of the ear should always be treated as serious. Tinnitus, or ringing in the ears, can result from damage to the hair cells of the organ of Corti. Damage to the auditory nerve can result in deafness. Upper respiratory infections can travel up the Eustachian tube and cause a common childhood infection of the middle ear known as "otitis media." Infections of the vestibular portion of the inner ear can result in recurrent or permanent dizziness (vertigo) because the inflamed cells transmit impulses that the body wrongly interprets as resulting from accelerations in unusual directions. Some plant poisons (or the drugs derived from them, such as ipecac) can also impair the function of the inner ear and result in sensations of dizziness, often followed by nausea and by the vomiting of the plant containing the poison. This reaction may have evolved as an adaptive response to possible poisons; the same reaction also results in vomiting in other situations that cause unusual accelerations in the vestibular portion of the inner ear, as in the case of seasickness or other motion sickness
.

A.D.A.M. Medical Encyclopedia. "Aging Changes in the Senses." MedlinePlus, November 11, 2012.

Agur, Anne M. R., and Arthur F. Dalley. Grant’s Atlas of Anatomy. 13th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013.

Ferrari, Mario. PDxMD Ear, Nose, and Throat Disorders. Philadelphia: PDxMD, 2003.

Møller, Aage R. Sensory Systems: Anatomy, Physiology, and Pathophysiology. 2d ed. Richardson, Tex.: Author, 2012.

Riordan-Eva, Paul, and John P. Whitcher. Vaughan and Asbury’s General Ophthalmology. 18th ed. New York: Lange Medical Books/McGraw-Hill, 2011.

Rosse, Cornelius, and Penelope Gaddum-Rosse. Hollinshead’s Textbook of Anatomy. 5th ed. Philadelphia: Lippincott-Raven, 1997.

Standring, Susan, et al., eds. Gray’s Anatomy. 40th ed. New York: Churchill Livingstone/Elsevier, 2008.

Sutton, Amy L., ed. Eye Care Sourcebook: Basic Consumer Health Information About Eye Care and Eye Disorders. 3d ed. Detroit, Mich.: Omnigraphics, 2008.

Wertenbaker, Lael T. The Eye: Window to the World. Reprint. New York: Scribner, 1984.

Whyche, Stephanie. "How the Five Sense Change with Age." InteliHealth, September 6, 2011.

What is kinesthetic memory? |

Introduction

Movement is central to sustaining life and fostering learning. Humans learn by kinesthetic, visual, or auditory methods, known as modalities, of processing sensory information. Each learning style engages a specific part of the brain to acquire, process, and store data. Educators develop teaching objectives compatible with students’ learning styles. Although the majority of people, approximately 65 percent, tend to learn best with visual memory, and 20 percent learn best through auditory memory, the 15 percent of humans who function best with kinesthetic memory usually retain information longer according to Bettina Lankard Brown for the Educational Resources Information Center (1998).

Kinesthetic memories are primarily stored in the cerebellum. This part of the brain has less risk for injury than the neocortex and hippocampus, which are involved in visual and auditory learning processes. Although kinesthetic memory is basic to the motions involved in writing, it is often ineffective for people attempting to comprehend academic topics. Kinesthetic types of learning are more suitable for mastering physical movements in sports and dance and in performance control such as playing instruments or singing.

Kinesthetic memory is fundamental to motor activity. Muscles in people and animals recall previous movements according to how body parts such as joints, bones, ligaments, and tendons interact and are positioned. This innate memory of relationships and sequences is the basis of motor skills such as writing or riding a bicycle. Because the brain relies on kinesthetic memory, it does not have to concentrate on how to move body parts. Instead, the brain can be focused for more complex thought processes and enhancement or refinement of movements.

Proprioception, the unconscious knowledge of body placement and a sense of the space it occupies, benefits from kinesthetic memory. Bodies are able to coordinate sensory and motor functions because of proprioception so that reflexes in response to stimuli can occur. These innate motor abilities help most organisms to trust that their bodies will behave as expected.

People have been aware of elements of kinesthetic memory since the late nineteenth century. Teacher Anne Sullivan used tactile methods to teach Helen Keller words. Keller, who was blind, deaf, and mute, touched objects, and kinesthetic sensations guided her to remember meanings. Educators have recognized the merits of kinesthetic learning to assist students, both children and adults, with reading difficulties. Kinesthetic memory has also been incorporated into physical therapies.

Measuring Memory

Kinesthetic memory is crucial for people to function proficiently in their surroundings. Measurement of kinesthetic memory is limited by clinical tools and procedures. Researchers are attempting to develop suitable tests to comprehend the role of kinesthetic memory in maintaining normal motor control for physical movement. Psychologists Judith Laszlo and Phillip Bairstow designed a ramp device that measures motor development and kinesthetic acuity in subjects’ upper extremities but not in specific joints. Kinesthetic acuity is how well people can describe the position of their body parts when their vision is obscured.

Some investigators considered Laszlo and Bairstow’s measurement method insufficient to examine some severely neurologically impaired patients, and it was revised to gauge nervous system proprioceptive deficiencies. Researchers at the University of Michigan-Flint’s Physical Therapy Laboratory for Cumulative Trauma Disorders adjusted ramp angles of laboratory devices in an attempt to create a better kinesthetic testing tool.

Kinesthetic studies examine such variables as gender and age and how they affect perception and short- and long-term kinesthetic memory. Results are applied to create more compatible learning devices and techniques that enhance information retention and recollection. Researchers sometimes assess how vibration of tendons and muscles or anesthesia of joints affects movement perceptions. Studies evaluate how kinesthetic stimuli affect awareness of size, length, and distance.

Kinesthetic memory tests indicate that kinesthetic performance varies according to brain characteristics and changes. Some tests involve tracing patterns at intervals during one week. Subjects are evaluated for how accurate their perceptions and memory of the required movements are from one testing session to the next. Such studies have shown that as people age, their kinesthetic memory capabilities decline. Mental health professionals seek treatment for brain injuries that result in ideomotor apraxia, a memory loss for sequential movements, and ideational apraxia, the breakdown of movement thought.

Intellectual Applications

Some educational specialists hypothesize that people with dyslexia
might lack sufficient kinesthetic memory to recognize and form words. Some dyslexia treatments involve strengthening neural pathways with physical activity to reinforce kinesthetic memory. As a result, some processes become instinctive and the brain can concentrate on understanding academic material and behaving creatively.

Teachers can help students acquire cursive handwriting skills by practicing unisensory kinesthetic trace techniques. Touch is the only sense students are permitted to use with this method, which develops kinesthetic memory for future writing. Blindfolded students trace letters with their fingers in a quiet environment. They repeat these hand and arm movements to form letters, then words. Muscular memories of these movements and body positions improve motor control for writing.

Kinesthetic-tactile methods are applied with some visual and auditory learning styles. In 1943 Grace Fernald introduced her method, VAKT, which used visual, auditory, kinesthetic, and tactile tasks simultaneously during stages of tracing, writing, and pronouncing. Margaret Taylor Smith established the Multisensory Teaching Approach (MTA). Beth Slingerland created the Slingerland Approach, which integrates all sensory learning styles, including kinesthetic motor skills.

Memorization is a fundamental part of musical activities. Singers rely on kinesthetic memory of throat muscles to achieve their desired vocal range and performance. Musicians develop kinesthetic memory skills by practicing pieces without visual cues to avoid memory lapses due to performance anxiety. Panic or nervousness can disrupt kinesthetic memories unless performers develop methods to deal with their fears or excitement.

Studies indicate that kinesthetic memory provokes signals that influence people’s memory. In particular, one study investigated how cues acquired during a learning process affect how people retain memories. Researchers focused on how people interacted with computers, specifically how the use of a pointing device, such as a mouse, and touchscreens affected retention of information viewed on computer screens. Pressing touchscreens, for instance, to control information contributed to increased spatial memory.

Body Intelligence

Kinesthetic memory guides children to develop control over their bodies. Jay A. Seitz, of York College/City University of New York, emphasizes that conventional intellectual assessments of children ignore bodily-kinesthetic intelligence. He argues that kinesthetic education, particularly in the mastery of aesthetic movements, is essential to balance traditional Western formal education, which focuses on cognitive linguistic and logical-numerical skills. Many educators consider those skills superior to other means of expressing intelligence. Seitz states that kinesthetic skills such as those developed by dance have significant cognitive aspects that can enhance academic curricula and children’s intellectual growth.

Jean Piaget
stressed that movement is an important factor in children’s early learning development. Infants’ sensorimotor experiences provide foundational knowledge for speech. Harvard University professor Howard Gardner built on Piaget’s premise by focusing on how people become skilled in coordinating their movements, manipulating items, and managing situations competently, what he terms bodily kinesthetic intelligence.

Kinesthetic memory is one of three main cognitive skills associated with bodily kinesthetic intelligence. Muscle memory allows people to use their bodies artistically to perform desired motion patterns, imitate movements, and create new nonverbal physical expressions. Motor logic and kinesthetic awareness supplement kinesthetic memory and regulate neuromuscular organization and presentation in such physical forms as rhythmic movement sequences and posture. Muscles and tendons have sensory receptors that aid kinesthetic awareness.

Seitz investigated how people use gestures to think and to express themselves. He emphasized that movement is the product of intellectual activity and can be recorded in kinesic language such as choreography, which describes dance sequences. Seitz conducted a qualitative and quantitative analysis of formal and informal dance classes to determine how children use kinesthetic sense and memory and motor logic to learn increasingly complicated dance routines. He noted that children aged three to four years have awareness of movement dynamics such as rhythm and balance.

After being taught simple choreography such as a butterfly-shaped pattern, children were asked to repeat the pattern five minutes later for a kinesthetic memory test. They were also asked to demonstrate a possible final gesture to a pantomime, such as pretending to throw a ball, as a motor logic test. The children were also shown pictures of people, structures, or items and asked to use their bodies to show what movements they associated with the images. All tests were videotaped to assess how children copied, created, or finished movements or the degree to which they failed.

Some children who lack motor skill competence have developmental coordination disorder (DCD), which was first classified in the fourth edition of the
Diagnostic and Statistical Manual of Mental Disorders
(1994, DSM-IV) and is included in the fifth edition, DSM-5. Authorities disagree whether DCD is caused by kinesthetic or visual perceptual dysfunction. Some tests reveal that children who have DCD might not kinesthetically rehearse memories they acquire visually. Laszlo and Bairstow developed kinesthetic sensitivity tests to assess subjects’ motor skills in processing information such as the position and movement of limbs. Kinesthetic perceptual problems result in clumsy movements. Therapists advocating the kinesthetic training approach encourage children to practice movements and develop better body awareness to refine motor skills.

Therapy

Kinesthetic memory contributes to physical fitness and the prevention of injuries. Researchers in the fields of kinesiology and biomechanics study how people move and incorporate kinesthetic concepts. Many athletes participate in Prolates, or progressive Pilates, which is a kinesthetically based conditioning program designed to achieve balance of muscle systems and body awareness of sensations and spatial location. Prolates practitioners view the human body as a unified collection of connected parts that must smoothly function together to achieve coordination, flexibility, and efficiency and to reduce stress.

This exercise program develops the mind-body relationship with movement visualization and concentration skills practice so people can instinctively sense how to fix athletic problems using appropriate muscles instead of repeatedly rehearsing mechanics. Prolates requires participants to achieve control of their center of gravity during diverse movements, thus refining kinesthetic memory. Athletes automatically adjust their physical stance when details about muscles are conveyed to the brain by proprioceptors, which are enhanced by Prolates.

Aquatic proprioceptive neuromuscular facilitation (PNF) is a movement therapy. This treatment helps fibromyalgia sufferers learn appropriate movement patterns to replace damaging behaviors such as clenching teeth, raising shoulders, and other excessive and unconscious muscle contractions and tensions that people use to deal with chronic pain and emotional stimuli. They also learn more efficient breathing techniques.

Erich Fromm encouraged the use of visual kinesthetic dissociation (V/KD), which is a therapy designed to help patients attain detachment from kinesthetic memories acquired traumatically, through physical abuse or rape. Therapists initiate V/KD by asking patients to act as observers, not participants, as though they are watching a movie, not acting in it, as they recall the traumatic experiences in their imagination. By paying attention to visual and auditory cues, patients gradually release kinesthetic memories. Sometimes, therapists ask the patients to play the scenes backward to reinforce nonkinesthetic memories and develop sensations of being empowered and competent.

Bibliography

Crawley, Sharon J. Remediating Reading Difficulties. 6th ed. New York: McGraw, 2012. Print.

Floyd, R. T. Manual of Structural Kinesiology. 18th ed. New York: McGraw, 2012. Print.

Jamison, Lynette, and David Ogden. Aquatic Therapy Using PNF Patterns. Tucson: Therapy Skill Builders, 1994. Print.

Laszlo, Judith I., and Phillip J. Bairstow. Perceptual Motor Behavior: Developmental Assessment and Therapy. New York: Praeger, 1985. Print.

Messing, Lynn, and Ruth Campbell, eds. Gesture, Speech, and Sign. Oxford: Oxford UP, 2004. Print.

Seitz, Jay A. “I Move . . . Therefore I Am.” Psychology Today 26.2 (1993): 50–55. Print.

Sheets-Johnstone, Maxine. "Kinesthetic Memory: Further Critical Reflections and Constructive Analyses." Body Memory, Metaphor, and Movement. Eds. Sabine C. Koch, Thomas Fuchs, Michela Summa, and Cornelia Muller. Vol. 84. Amsterdam: Benjamins, 2012. 43–72. Print.

Wing, Alan M., Patrick Haggard, and J. Randall Flanagan, eds. Hand and Brain: The Neurophysiology and Psychology of Hand Movements. San Diego: Academic, 1996. Print.

What do the lines of Bob Dylan's "Blowing in the Wind" mean?

"Blowing in the Wind" has multiple interpretations.  It changed the music scene as it appeared on the radio at a time when it was dominated by pop songs such as "Candy Girl" by the Four Seasons.  When Dylan released this on his 1963 album Freewheelin' Bob Dylan, he did not intend for it to have any meaning at all, but the meaning is out there--"blowing in the wind."  War protesters later in the decade listened...

"Blowing in the Wind" has multiple interpretations.  It changed the music scene as it appeared on the radio at a time when it was dominated by pop songs such as "Candy Girl" by the Four Seasons.  When Dylan released this on his 1963 album Freewheelin' Bob Dylan, he did not intend for it to have any meaning at all, but the meaning is out there--"blowing in the wind."  War protesters later in the decade listened to the song and said that it was a peace ballad when in the first stanza Dylan mentioned "banning cannonballs."  Civil rights' marchers said the song was for them when in that same stanza Dylan mentions, "How many roads must a man walk down / Before you call him a man?"  Yet there are other people who appreciate the simple lyrics, tune, and imagery who think that Dylan paints a lovely word picture.  In a later interview, Dylan himself said that the song was not meant to be specifically for any one group.  The song has since been recorded by other artists including Peter, Paul, and Mary.  

What is Parkinson's disease? |

Causes and Symptoms

In 1817, James Parkinson, a British physician, wrote a description of six patients
suffering from a slowly progressing disease characterized by “involuntary
tremulous motion, with lessened muscular power in parts not in action even when
supported, with a propensity to bend their trunks forward from a walking to a
running pace.” Throughout the modern world, this disease—which Parkinson named
shaking palsy—is called Parkinson’s disease.

Parkinson’s disease, also called paralysis agitans, is now defined as a medical
condition characterized by a combination of symptoms including involuntary shaking
(tremor) of the limbs at rest, stiffness of the muscles
(rigidity), slowed or reduced ability to move the limbs and facial muscles
(bradykinesia), and general muscular weakness. Onset usually occurs after the age
of fifty.

The clinical scale most often used to describe the extent of severity of
Parkinson’s disease is that of Melvin Yahr and Margaret Hoehn, which is divided
into five stages. In stage 1, mild tremor or rigidity is seen on one side of the
body. In stage 2, tremor, rigidity, and bradykinesia occur on both sides of the
body, without any loss of balance. In stage 3, added to the symptoms of stage 2
are balance difficulty, loss of posture control, and hunching over. With stage 4,
the extent of the functional disability increases, but some independent function
is still possible. Such severe symptoms occur in stage 5 that patients require a
wheelchair or are bedridden without assistance.

The body site of Parkinson’s disease is clear, but most cases are idiopathic,
meaning that although their site of action is known, the basic cause is not and
their occurrence is spontaneous. Parkinson's disease is estimated to have a 30 to
40 percent rate of heritability. Mutations in the parkin (PARK2)
gene on chromosome 6 are found in approximately 8.6 percent of patients with
early-onset Parkinson's disease; researchers have identified more than two hundred
PARK2 gene mutations involved in the development of
Parkinson's disease. Multiple genes may be involved in idiopathic late-onset
Parkinson's disease; the tau gene is being investigated as a possible cause of
idiopathic Parkinson's disease.

Although a genetic susceptibility may be responsible for some cases of
Parkinson's, many researchers increasingly believe that the root of Parkinson’s
disease is related to environmental factors. While a handful of gene mutations
have been identified for early-onset Parkinson’s, which strikes before the age of
forty, these cases account for fewer than one out of every ten patients. Some
scientists believe that the genes involved in Parkinson's may be “activated” by
exposure to an environmental agent, such as solvents, pesticides, or viruses, and
that such agents may prompt the onset of the disease even in those individuals who
carry none of the suspected genes. Recent findings seem to support such expert
hypotheses. For example, common clusters of individuals with the disease have been
discovered, most notably three people who worked in Canada during the 1980s with
Michael J. Fox, the television and film actor who announced in 1998 that he was
suffering from Parkinson’s disease. Medical detectives are examining whether any
shared environmental exposure among this group of four can be found. Moreover,
Japanese scientists showed that a virulent strain of influenza A accumulates in
the same area of the brain attacked in Parkinson’s disease. Other studies have
shown that health care workers and teachers, individuals in fields exposed at a
greater rate to influenza strains, show a twofold increased risk of
developing the disease. Finally, epidemiological studies show that people living
in rural areas and farmers are much more likely to develop the disease than their
urban counterparts, a fact that could point to pesticide exposure or the use of
well water.

The symptoms of Parkinson’s disease begin slowly, most often presenting as stage 1
tremor. After this, the progression to stage 3 usually takes five to ten years.
This progression appears to be caused by the deterioration of several of the four
brain structures called basal ganglia (the corpus striatum, thalamus, substantia
nigra, and globus pallidus), which is related to depletion of the neurotransmitter
dopamine. Dopamine depletion is most extreme in the normally dark-pigmented
substantia nigra, which is often colorless in the autopsied brains of parkinsonism
patients.

The side effects of some drugs can produce symptoms of Parkinson’s disease that
are difficult to distinguish from non-drug-induce Parkinsonism, and they have
provided clues about the disease. Many of these drugs affect dopamine levels in
the brain and include antipsychotic medications, metoclopramide, reserpine,
tetrabenazine, some calcium channel blockers, and stimulants such as amphetamines
and cocaine. Drug-based symptoms do not appear to be causes of permanent
Parkinson’s disease because the symptoms diminish and slowly disappear after
discontinuation of the causative drugs. Many have been linked, however, to
decreased dopamine levels. Similarly, many stroke-related symptoms appear to be
caused by drug therapy that diminished brain dopamine content. The effects of
tumors have also offered helpful data because their location
can better identify the brain areas associated with the disease. For example,
information of this sort first linked the substantia nigra and corpus striatum to
Parkinson’s disease. In addition, viral encephalitis is still suspected by many of
being an important causative factor. Belief in its involvement arose, however,
from a 1918–1925 epidemic that damaged the basal ganglia, and contemporary
Parkinson’s disease as a result of encephalitis is very rare. Finally, discovery
of the MPTP connection, a neurotoxin precursor to MPP+, has yielded a useful model
for Parkinson’s disease related to psychoactive drugs that cause it.

Tremor is the most conspicuous symptom. Despite the fact that it is usually the
least disabling aspect of the disease, tremor is often embarrassing to the
affected person and it is usually the phenomenon that brings patients to a
physician for initial diagnosis. In stage 1 of Parkinson’s disease, tremor appears
only when afflicted people are very fatigued. Later in the course of the disease,
it becomes increasingly widespread and continual. It is interesting to note that
tremor ceases when a parkinsonism patient is asleep.

Although Parkinson’s disease does not alter the mental abilities of afflicted
persons, it eventually impairs their ability to carry out tasks that require
rapid, repetitive movement and manual dexterity. For example, Parkinson’s disease
very often causes handwriting to deteriorate to an illegible scrawl, makes it
impossible to fasten a shirt’s collar buttons or a brassiere, and turns shaving or
brushing the teeth into a difficult chore.

Bradykinesia is the most incapacitating aspect of Parkinson’s disease because it
impairs communication by characteristic gestures; results in an awkward gait, with
failure to swing the arms normally when walking; and produces an immobile facial
expression common to later stages. Other symptoms include drooling, caused by
problems with swallowing, and the development of a slow, muffled speech. Both are
caused by diminished mobility of the muscles of the mouth, jaws, and throat.

The nature of Parkinson’s disease is best understood after considering nerve
impulse transmission between the cells of nervous tissue (neurons) and the
arrangement and interactive function of the brain and nerves.

Nerve impulse transport between neurons is an electrochemical process that
generates the weak electric current that makes up the impulse. The impulse leaves
each neuron via an outgoing extension, called an axon, passes across a tiny
synaptic gap that separates the axon from the next neuron in line, and then enters
an incoming extension (dendrite) of that cell. This process is repeated many times
in order to transmit a nervous impulse to its site of action. The cell bodies of
neurons constitute the impulse-causing gray matter, and axons and dendrites (white
matter) may be viewed as their connecting wires (nerve fibers). Nerve impulse
passage across the synaptic gaps between neurons is mediated by chemical
messengers called neurotransmitters, such as dopamine.

The brain and nerves—the central nervous system—are a complex arrangement of
neurons designed to enable an organism to respond in a coordinated way to external
stimuli. The brain may be viewed as the central computer in the system. Its most
sophisticated structure is the cerebrum, which controls the higher mental
functions. Underneath the cerebrum are the cerebellum and the brain stem, which
connects both the cerebrum and the cerebellum to the spinal cord.
This cord, a meter-long trunk of nerve fibers, carries nerve impulses between the
brain and the peripheral nerves that control muscles and other body tissues. Most
important to Parkinson’s disease are the motor nerves, which control body motions.
This control involves a portion of the cerebrum that deals with skilled motor
patterns; the cerebellum, which controls posture and balance; and the basal
ganglia, which are processing centers for movement information.

Particularly important to Parkinson’s disease are the substantia nigra and the corpus striatum. Discovery of a functional interface between dopamine and Parkinson’s disease began when it was found that this neurotransmitter was associated with the substantia nigra and connected the substantia nigra and the corpus striatum. Next, it was discovered that temporary Parkinson’s disease mediated by reserpine was associated with dopamine depletion and that the brains of patients contained very little dopamine in the substantia nigra. Soon, it was confirmed that dopamine controlled movement in an inhibitory fashion that arose in the substantia nigra and occurred in the corpus striatum. From these observations, it has been inferred that bradykinesia results from the damage of the dopamine-containing nerve tissue that connects the substantia nigra to the corpus striatum. It is also suggested that decreased function of these fibers—and lack of their inhibitory action because of dopamine—allows excess, undesired nerve impulses to cause both the tremor and the rigidity seen in Parkinson’s
disease.

Treatment and Therapy

Parkinson's disease can be difficult to diagnose, particularly in the early
stages. Parkinson’s disease is most often identified by physical evidence (such as
tremor and bradykinesia), coupled with a careful study of the medical history of
the patient being evaluated. In all but a few cases, no diagnostic information can
be obtained via the three powerful tools useful in many other neurologic exams:
The complex X-ray method, computed tomography (CT) scanning, is
informative only when stroke or tumor is involved; magnetic resonance imaging
(MRI) gives no more information than do CT scans; and electroencephalograms (EEGs)
do not show abnormal electrical discharge such as that observed in brains of
patients with epilepsy. In practice, however, many physicians carry out CT scans,
MRI, and EEGs and count their negative results into a diagnostic positive for
Parkinson’s disease.

Once Parkinson’s disease is diagnosed, three main methods exist for managing it:
medications, physical therapy, and surgery. All these methods—alone or in
combination—are intended for symptom reversal because there is no cure for the
disease. Medications are the first-line treatment mode in most cases. Many
different medications are used, such as levodopa (L-Dopa), dopamine agonists,
monoamine oxidase type B inhibitors, and anticholinergic drugs.

The anticholinergics were the first drugs used for Parkinson’s disease, and they
are still often prescribed for younger patients with severe tremors, but they are
now associated with limited efficacy and neuropsychiatric side effects. The first
anticholinergic drug used, in the 1890s, was scopolamine, initially isolated from
Datura stramonium (jimsonweed). Other anticholinergics include
atropine and the antihistamine diphenhydramine (Benadryl). These drugs operate by
interfering with the action of acetylcholine, a neurotransmitter
involved in nerve impulse transport. High doses of anticholinergic drugs produce
many side effects, including confusion, slurred speech, blurred vision, and
constipation because of the wide influence of cholinergic nerves on body
operation.

Levodopa, the amino acid that is made into dopamine by the body, is a first-line
choice in the treatment of Parkinson's. Levodopa is a metabolic precursor of
dopamine and can improve motor impairment. Dopamine itself is not used because a
blood-brain barrier prevents brain dopamine uptake from the blood. The blood-brain
barrier does not stop levodopa uptake, and its administration reverses symptoms
dramatically. Therefore, it has become the mainstay of modern chemotherapy for the
disease.

A difficulty associated with use of levodopa is that the biochemical mechanism
that converts it to brain dopamine also occurs outside the brain. When this
happens in patients given high doses of levodopa, body (nonbrain) dopamine levels
rise. This dopamine and the chemicals into which it transforms outside the brain
cause such side effects as nausea, fainting, flushing, confusion, and the
involuntary muscular movements called dyskinesia. The dose should be kept low
to maintain function and reduce motor complications. To minimize these
unwanted—and sometimes irreversible—side effects, modern levodopa therapy
sometimes combines the drug with its chemical cousin, carbidopa. Carbidopa
prevents the conversion of levodopa to dopamine. Because it cannot cross the
blood-brain barrier, carbidopa has no effect on the brain’s conversion of levodopa
to dopamine.

Another first-line medication for treating Parkinson’s disease is dopamine
agonists. These chemicals mimic dopamine action, reacting with the brain’s
receptors that produce dopamine effects in the corpus striatum and other sites.
Monoamine oxidase type B (MAO-B) inhibitors may be used for patients with early
disease. MAO-B inhibitors such as selegiline can delay the onset of motor
complications compared to levodopa but may be less effective in the treatment of
functional impairment.

Furthermore, it is not uncommon for those afflicted with Parkinson’s disease to
suffer from depression as they lose control of their motor functions.
This is probably the case because, as noted by James Parkinson, “the senses and
intellect are unimpaired” in such patients. However, traditional antidepressants
may not reduce depression in patients with Parkinson's disease, and several
antidepressant medications can have negative interactions with the medical
treatment of Parkinson's. Pramipexole, a dopamine agonist, is associated with
improvement in depressive symptoms in patients with Parkinson's disease.
Venlafaxine, an antidepressant and serotonin-norepinephrine reuptake inhibitor,
may also be used in the treatment of depression in patients with Parkinson's.

Surgical treatment of Parkinson’s disease was once attempted quite often, but it
became relatively rare by the 1970s, after modern medications were developed.
Since then, its utilization occurs when CT scanning or MRI indicates the presence
of a tumor or brain damage caused by a severe trauma. An implant that provides
deep brain
stimulation has been used to suppress tremors and improve
quality of life. Thalamotomy, the destruction of the thalamus—the brain region
that controls some involuntary movements, was also once more commonly used in the
surgical treatment of Parkinson's, but it is a highly invasive procedure and it is
only rarely used for the treatment of severe drug-resistant tremors. More
recently, thalamic stimulation appears to be as effective as thalamotomy with
fewer adverse effects.

Two final topics worth mentioning are cognitive-behavioral therapy and physical
therapy. Part of their purpose is to address the depression that often accompanies
severe Parkinson’s disease. Cognitive-behavioral therapy for Parkinson's diseases
often includes exercise, behavioral activation, thought monitoring and
restructuring, relaxation training, worry control, and sleep hygiene.
Cognitive-behavioral therapy provides emotional support to patients with
Parkinson's and has been found to improve global symptom severity. Physical
therapy can help patients to overcome some motor effects of the disease, not only
improving the lifestyle possible for them but also elevating morale and curing
depression. Endurance exercises and progressive resistance exercises have been
found to improve physical performance in patients with Parkinson's disease.

Perspective and Prospects

Treatment of Parkinson’s disease has evolved tremendously, particularly since the
late 1960s, when wide use of levodopa began. At that time, most physicians were
astounded to observe that its use converted many stage-5 patients, who were
bedridden or wheelchair-bound, to much more functional, mobile states. A temporary
setback occurred when severe levodopa side effects were observed at high
doses.

The discovery of carbidopa and related inhibitors of nonbrain dopamine
decarboxylase ended this problem and produced a new generation of chemotherapy.
Patients could take levodopa at lower concentrations, which minimized its side
effects, because diminished nonbrain levodopa conversion to dopamine left more
levodopa available to enter the brain. In addition, carbidopa was the forerunner
of a group of dopamine agonists that became candidates for independent use or use
in mixed therapy.

Researchers at the turn of the twenty-first century closely examined the genetic
links in familial forms of Parkinson’s disease. One gene, α-synuclein, is a
presynaptic neuronal protein that is believed to play a significant role in
neuronal plasticity. α-synuclein was previously associated with Alzheimer’s
disease as the nonamyloid component of Alzheimer’s amyloid plaques (NAC peptide),
and it is a component of the Lewy inclusion bodies found in the
Parkinson’s-associated Lewy body dementia. Mutations in another gene, Parkin
(PARK2), were found to underlie the development of
juvenile-onset Parkinson’s disease. Parkin is believed to play a role in cellular
protein degradation by interacting with ubiquitin, a protein that targets other
proteins for degradation. It is hoped that the identification of these genes will
lead to a better understanding of the pathogenic mechanisms underlying nonfamilial
(sporadic) Parkinson’s disease.

Discovery that cognitive-behavioral therapy and exercise can ease the depression
observed in many afflicted people and help to control the disease’s progression
has also been of great value. Perhaps even more exciting have been reports that
the injection of human fetal cells into the brains of those afflicted with
Parkinson’s disease may be able to reverse the disease. It is too soon, however,
to judge the results of this procedure.

Bibliography

Gordin, Ariel, Seppo
Kaakkola, and Heikki Teräväinenet, eds. Parkinson’s
Disease. Philadelphia: Lippincott, 2003. Print.

Lieberman, Abraham N.
One Hundred Questions and Answers About Parkinson
Disease. Sudbury: Jones, 2003. Print.

Lima, Lidiane Oliveria, Aline Scianni, and
Fatima Rodrigues-de-Paula. "Progressive Resistance Exercise Improves
Strength and Physical Performance in People with Mild to Moderate
Parkinson's Disease: A Systematic Review." Journal of
Physiotherapy 59.1 (2013): 7–13. Print.

Marras, Connie, et al. "Systematic Review of
the Risk of Parkinson's Disease after Mild Traumatic Brain Injury: Results
of the International Collaboration on Mild Traumatic Brain Injury
Prognosis." Archives of Physical Medicine and
Rehabilitation 95.3 (2014): S238–S244. Print.

Martinez, Ana, and Carmen Gil, eds.
Emerging Drugs and Targets for Parkinson's Disease.
Cambridge: RSC, 2013. Print.

Nicholls, John G., A.
Robert Martin, and Bruce G. Wallace. From Neuron to Brain.
5th ed. Sunderland: Sinauer, 2011. Print.

Parkinson’s Disease Foundation. http://www.pdf.org.

Paul, S . S., et al. "Leg Muscle Power Is
Enhanced by Training in People with Parkinson's Disease: A Randomized
Controlled Trial." Clinical Rehabilitation 28.3 (2014):
275–88. Print.

Pfeiffer, Ronald F., Zbigniew K. Wszolek,
and Manuchair Ebadi, eds. Parkinson's Disease. 2nd ed. Boca
Raton: CRC, 2013. Print.

Physicians’ Desk Reference. 65th ed. Montvale: PDR Network,
2011. Print.

Porter, Robert S., et
al., eds. The Merck Manual of Diagnosis and Therapy. 19th
ed. Whitehouse Station: Merck Research Laboratories, 2011. Print.

Schwartz, Shelley
Peterman. Three Hundred Tips for Making Life with Parkinson’s
Disease Easier. New York: Demos Medical, 2002. Print.

Yoshida, Chiyo, and Ami Ito, eds.
Parkinson's Disease: Diagnosis, Treatment and Prognosis.
New York: Nova, 2012. Print.

What is inositol as a dietary supplement?

Overview

Inositol, unofficially referred to as vitamin B8, is present in all animal tissues, with the highest levels in the heart and brain. It is part of the membranes (outer coverings) of all cells. It plays a role in helping the liver process fats and in contributing to the function of muscles and nerves.

Inositol may also be involved in depression. People who are depressed
may have lower-than-normal levels of inositol in their spinal fluid. In addition,
inositol participates in the action of serotonin, a neurotransmitter known to be a
factor in depression. (Neurotransmitters are chemicals that
transmit messages between nerve cells.) For these two reasons, inositol has been
proposed as a treatment for depression, and preliminary evidence suggests that it
may be helpful. Inositol also has been tried for other psychological and
nerve-related conditions.

Sources

Inositol is not known to be an essential nutrient. However, nuts, seeds, beans, whole grains, cantaloupe, and citrus fruits supply a substance called phytic acid (inositol hexaphosphate, or IP6), which releases inositol when acted on by bacteria in the digestive tract. The typical American diet provides an estimated 1,000 milligrams daily.

Therapeutic Dosages

Experimentally, inositol dosages of up to 18 grams (g) daily have been tried for various conditions.

Therapeutic Uses

Inositol has been studied for depression, bipolar disorder, panic disorder, bulimia, and obsessive-compulsive disorder, but the evidence remains far from conclusive. Other potential uses include Alzheimer’s disease and attention deficit disorder. According to two double-blind studies enrolling almost four hundred people, inositol may help improve various symptoms of polycystic ovary syndrome, including infertility and weight gain. Another small double-blind study found that inositol supplements could help reduce symptoms of psoriasis triggered or made worse by the use of the drug lithium. A small double-blind study failed to find inositol helpful for premenstrual dysphoric disorder, a severe form of premenstrual syndrome.

Inositol is sometimes proposed as a treatment for diabetic neuropathy, but there have been no double-blind, placebo-controlled studies on this subject, and two uncontrolled studies had mixed results. Inositol has also been investigated for potential cancer-preventive properties.

Scientific Evidence

Depression. Small double-blind studies have found inositol helpful for depression. In one such trial, twenty-eight depressed persons were given a daily dose of 12 g of inositol for four weeks. By the fourth week, the group receiving inositol showed significant improvement compared with the placebo group. However, a double-blind study of forty-two people with severe depression that was not responding to standard antidepressant treatment found no improvement when inositol was added.

Panic disorder. People with panic
disorder frequently develop panic
attacks, often with no warning. The racing heartbeat, chest
pressure, sweating, and other physical symptoms can be so intense that they are
mistaken for a heart attack. A small double-blind study (twenty-one participants)
found that people given 12 g of inositol daily had fewer and less severe panic
attacks compared with the placebo group.

A double-blind, crossover study of twenty people compared inositol to the
antidepressant drug fluvoxamine (Luvox), a medication related to Prozac. The
results of four weeks of treatment showed that the supplement was, at minimum,
just as effective as the drug.

Bipolar disorder. In a six-week, double-blind study, twenty-four
people with bipolar disorder received either placebo or inositol (2 g
three times daily for a week, then increased to 4 g three times daily) in addition
to their regular medical treatment. The results of this small study failed to show
statistically significant benefits; however, promising trends were seen that
suggest a larger study is warranted.

Polycystic ovary syndrome. Polycystic ovary syndrome
(PCOS) is a chronic endocrine disorder in women that leads to
infertility, weight gain, and many other problems. In a double-blind,
placebo-controlled trial, 136 women with PCOS were given inositol at a dose of 100
mg twice daily, while 147 were given placebo. During the study period of fourteen
weeks, participants given inositol showed improvement in ovulation frequency
compared with those given placebo. Benefits were also seen in terms of weight loss
and levels of HDL (good) cholesterol. A subsequent study of ninety-four women
found similar results. However, both of the studies were performed by the same
research group. Independent confirmation is necessary before inositol can be
considered an effective treatment for PCOS.

Safety Issues

No serious side effects have been reported for inositol, even with a therapeutic dosage that equals about eighteen times the average dietary intake. However, no long-term safety studies have been performed.

Although inositol has sometimes been recommended for bipolar disorder, there is evidence to suggest inositol may trigger manic episodes in people with this condition. Persons with bipolar disorder should not take inositol unless under a doctor’s supervision.

Safety has not been established in young children, women who are pregnant or nursing, and those with severe liver and kidney disease. As with all supplements used in very large doses, it is important to purchase a reputable product, because a contaminant present even in small percentages could be harmful.

Bibliography

Allan, S. J., et al. “The Effect of Inositol Supplements on the Psoriasis of Patients Taking Lithium.” British Journal of Dermatology 150 (2004): 966-969.

Gerli, S., et al. “Randomized, Double-Blind, Placebo-Controlled Trial: Effects of Myo-Inositol on Ovarian Function and Metabolic Factors in Women with PCOS.” European Review for Medical and Pharmacological Sciences 11 (2007): 347-354.

Nemets, B., et al. “Myo-Inositol Has No Beneficial Effect on Premenstrual Dysphoric Disorder.” World Journal of Biological Psychiatry 3 (2002): 147-149.

Palatnik, A., et al. “Double-Blind, Controlled, Crossover Trial of Inositol Versus Fluvoxamine for the Treatment of Panic Disorder.” Journal of Clinical Psychopharmacology 21 (2001): 335-339.

What is sibling rivalry? |

Causes and Symptoms

Sibling rivalry is the competition or jealousy that develops between siblings for the love, affection, and attention of either one or both parents. The concept of sibling rivalry has been discussed for centuries, and it is considered a universal phenomenon in families. Although sibling rivalry is generally described in terms of its negative aspects, healthy competition between brothers and sisters can be useful in the individual development of necessary social, communication, and cognitive skills.

While the dynamics of the ways in which brothers and sisters relate to one another cannot be reduced to specifics of age, birth order, gender, and family size, these family constellation variables are important in the development of sibling rivalry. While each element will be discussed separately, it is important to take into account all the relevant factors when looking at causes of sibling rivalry.

The ages of siblings and their birth order are significant factors that have been related to sibling competition. There are many stereotypes associated with being the oldest, youngest, and middle child in the family. For example, typical firstborn children tend to be highly organized and responsible, while youngest children are likely to benefit from more experienced, relaxed parenting and may be more affectionate and spontaneous. Middle children are often more difficult to characterize. They may be at more risk than other children for receiving less attention, and they tend to develop stronger relationships outside the family. Using these stereotypical characteristics as guides for assessing a particular child, it is possible to speculate on the relevance of birth order and age in the development of sibling competition.

The effects of spacing between children has also given rise to a number of theories. It is generally accepted that the closer siblings are in age, the more similar their life experiences are likely to be. As they may have more in common, siblings close in age are also more likely to struggle with each other more frequently. For this reason, siblings who are close in age may engage in more competition with each other than siblings who are separated by more than a few years.

The gender of siblings is also a variable in the development of sibling relationships, including sibling competition. Siblings help each other discover some of the basic characteristics of male and female roles. Growing up with all brothers or all sisters can teach a child much about dealing with one gender. Having a sibling of the opposite sex can offer a child valuable initial information about the opposite sex. The attitudes of parents regarding gender roles also influence the relationships between siblings. Parents who display favoritism toward children based on gender may contribute to sibling jealousy and competition.

For a wide variety of reasons, specific children may be more emotionally vulnerable to feelings of jealousy than their siblings at a given time. For example, in a family with a child who has a disability, other siblings may feel that they do not receive as much attention, or the child with special needs may feel different and unwanted.

Emotionally vulnerable children are frequently found in families experiencing high levels of stress. There is evidence that the emotional climate within the family is directly linked to the quality of sibling relationships. It then follows that sibling rivalry may be more problematic in families where there are stressors such as marital conflict, chronically ill family members, or unwanted extended family involvement.

The competition that emerges between siblings can be for material resources such as toys or space within the household. For example, it is not uncommon for an older child to resent having to share a room with a younger brother or sister. Frequently, the competition for material resources stems from a child’s uncertainty regarding his or her status in the family. Children may interpret the need to share space as an indication of their lesser importance to parents.

Jealousy can develop when a child perceives favoritism on the part of a parent. This jealousy results from a lack of equality in treatment. Not only is the less favored child at risk for feeling jealous, but the parental favorite often does not perceive the extra attention as pleasant or comfortable. The challenge in parenting is trying to achieve equality when children are each exceptional beings with their own individual needs. In her book Dr. Mom’s Parenting Guide (1991), Marianne Neifert recommends loving children “uniquely,” giving each child the message that his or her place in the family is a special one. A parent who consistently favors one child over another through the amount of love and attention shown is encouraging unhealthy rivalry between the children.

Sibling rivalry can manifest itself in a variety of ways. When a new sibling is born, an older child may be either openly or passively hostile to the new baby. This hostility can be displayed in the form of direct verbal or physical attacks on the baby. Sometimes children request that parents return the infant to the hospital or give it away. In other cases, a child may act up or demand attention when the parent is busy with the infant. Serious abuse by siblings is rare, but even mild incidents need attention by parents.

Some children react to a new sibling by displaying regressive behavior such as bed-wetting, asking to be carried, thumb-sucking, excessive crying, or talking baby talk. Other negative behaviors associated with sibling jealousy are lying, aggressiveness, or destructive behaviors. It is also typical for the child to vent frustration or anger on other individuals, pets, or toys when feeling jealous of a sibling. In older children, sibling rivalry may be exhibited by taking the younger child’s toys or demanding more parental attention. Another example of rivalry in older children includes a drive to outperform the other sibling in academic or athletic settings.

Unless managed effectively by parents, feelings of jealousy and competition among siblings can undermine a child’s development and may continue into adult relationships. Sibling rivalry can be minimized by the active involvement of parents in setting appropriate rules for dealing with conflicts.

Treatment and Therapy

The negative impact of sibling rivalry can be minimized through parental education and attention to the conditions that intensify sibling competition. Attending to the development of a relationship between siblings is an ongoing process that parents can enhance through their involvement in helping children develop good interpersonal skills.

The foundation for dealing effectively with sibling rivalry is an awareness and understanding that sibling competition is a normal, healthy part of family life. Rivalry develops between siblings in nearly every family, and it becomes problematic only when taken to extremes or when ignored and allowed to escalate.

The common behavior problems associated with sibling rivalry occur in the context of many interacting factors: parental expectations; the child’s developmental level; the temperament of a particular child; parental discipline; family constellation characteristics such as age, gender, and spacing of children; and the presence of extended family members. There is growing evidence regarding the importance of obtaining assessments and information from family members (including extended family) and other sources such as school or day care personnel when identifying a problem of sibling rivalry.

One of the situations in which parents express the most open concern regarding sibling rivalry is when a new baby is expected or an adoption of a child is imminent. When a new sibling is expected, the other children can be invited to be actively involved in the preparation. Age-appropriate discussions with each child about pregnancy or adoption are good preventive measures. Parents should be available to answer questions regarding the changes to be expected with the arrival of the additional child. An open, direct discussion with older children can minimize the adjustment difficulties and address initial concerns. Children need regular verbal and demonstrated assurances that they will continue to be loved following the arrival of a new sibling.

Parents can involve an older child in the care of a baby as a means of acknowledging the unique contributions of that child. Expecting an older child to be a regular caretaker, however, may create additional problems and place unnecessary stress on the older brother or sister.

While some older children exhibit negative behaviors associated with the arrival of a baby, others respond positively by becoming more mature and autonomous. Focusing on the individual contributions of an older sibling can minimize the feelings of jealousy when a new child enters the family.

Parents should avoid making either overt or subtle comparisons between siblings and instead focus on the special qualities and achievements of each child. As Neifert suggests, “honor the individual in every child.” This is sometimes difficult to accomplish, as many times parents anticipate that subsequent children will be similar to their firstborn. For example, if a first child is successful in sports, a parent may anticipate that the younger sibling will also be athletically inclined. Such unrealistic expectations can foster unhealthy competition and put needless pressure on a younger sibling.

Jealousy between brothers and sisters seldom ends with the adjustment of a new family member and the acknowledgment that an “only” child now has to share parental attention. Balancing the emotional needs of two or more children of differing ages continues to be an important concern of parents as children move through different developmental stages.

The negative behaviors associated with sibling rivalry can stem from other sources as well. Sometimes siblings fight because they are bored or have few appropriate alternatives to taunting a sibling. Sometimes the behavior can be a reaction to stressors outside the home, such as problems at school or socialization difficulties. A parent’s reaction to negative behavior will have a large impact on whether the behavior continues. Parents who can model effective interpersonal skills themselves are likely to influence the development of these same skills in their children.

When jealous behaviors are displayed by siblings, parents need to be sensitive to the source of the feelings. The cause of the competition or rivalry should be the focus of parental interventions, rather than the negative behavior itself. Children should be encouraged to talk about their feelings openly, and parents need to be willing to acknowledge and validate those feelings for each child. After allowing children to express their feelings and showing appreciation for the difficulty of the problem, parents can encourage siblings to work toward a mutual resolution.

One of the common manifestations of sibling rivalry is the expression of anger and, sometimes, the physical or verbal abuse that accompanies the anger. While common, violent displays of anger are not appropriate. Helping children learn to handle anger responsibly is an important task for parents.

In handling fighting between children, parents must assess the level of conflict and intervene appropriately when necessary. Normal bickering between siblings that does not include verbal abuse or threats of physical abuse rarely requires parental involvement. If the situation worsens, however, the following steps can be useful for parents: acknowledge the angry feelings of each child, then reflect each child’s point of view; describe the problem from the position of a respectful bystander, without taking sides on the issue; and express confidence that the children can come up with a reasonable solution.

Parents need to be actively involved in promoting a system of justice within the family that includes age-appropriate rules and consequences for behavior. Examples of ways that parents can manage the behavior are separating siblings when a situation appears dangerous and redirecting children’s activities when aggression is likely to occur. Parents can also take responsibility for encouraging and rewarding cooperative play and for providing children with appropriate, nonaggressive models for resolving conflict.

Teaching children conflict resolution strategies is an important way for parents to intervene in sibling rivalry problems. Developing the ability to express one’s feelings is a valuable step toward conflict resolution. Children should be encouraged to put their feelings into words in appropriate ways. Young children may need help in doing so through the use of statements such as, “You don’t like it when I spend so much time caring for your baby sister, do you?” Granting a child permission to fantasize about a given situation may also help in diffusing angry feelings. Encouraging children to verbalize what they wish would happen allows them to address emotions in an honest way. Children should be taught from an early age to develop creative ways to vent their anger. Children can be taught to use physical exercise, write feelings in a journal, or go to their rooms to cool down as appropriate ways to manage anger.

Managing sibling conflict is complex in any family, but even more so in situations where there is a single parent or a blending of families through divorce and remarriage. Because sibling competition stems from a child’s anxiety about sharing parental attention, the presence of a single parent can intensify the feelings of insecurity about one’s position in the family. Single parents need to be careful not to turn a child into a spouse substitute, instead viewing each child as a unique individual who deserves to be able to mature at his or her own pace. Extended family members, including grandparents, aunts, and uncles, may be useful in helping a single parent meet the individual needs of each child in the family.

When parents remarry, children are required to make adjustments in their relationships and to include new people in their family. Children need to be allowed to express their ambivalent feelings regarding stepsiblings and half siblings, as these feelings are a normal part of this adjustment process. Parents need to accept and tolerate each child’s feelings, as long as guidelines of justice and safety are recognized.

Childhood rivalries between siblings can be revived in adulthood, especially when children must come together to make decisions about aging parents. Feuds erupt easily between brothers and sisters over complicated issues such as who should have the most control over belongings, medical care, and finances. In some cases, rivalries are increased when the decision is made to take the parent in to one of the siblings' home rather than place him or her in a care facility.

Despite the abundant research available on the topic of sibling rivalry, there is still much that is unknown regarding the complex relationships between brothers and sisters. While it is possible to look at generalizations regarding the issues important in sibling rivalry, it is not possible to predict adjustment or maladjustment in a particular child. Information must be gathered from a number of sources and evaluated for each child when planning a course of action to address concerns about sibling rivalry.

Perspective and Prospects

Through the ages, people have assumed that jealousy and rivalry are unavoidable characteristics of sibling relationships. Sibling rivalry is a common theme in several classic stories. In the Bible, the competition between brothers Cain and Abel and the jealousy that develops between Joseph and his brothers over issues of parental favoritism are but two accounts of sibling rivalry. Such accounts support the assertion that jealousy among siblings is a common phenomenon.

Sigmund Freud’s theory of socialization was one of the first to address the concept of sibling rivalry from a scientific perspective. According to Freud, sibling rivalry, with its struggles and controversy, is inherent in all brother-and-sister relationships. Much of what Freud hypothesized regarding sibling competition was grounded in a personal understanding of his own relationships with his siblings. Freud was the oldest child in a family that included five younger sisters and a younger brother.

Competition for parental attention is a dominant theme in Freud’s description of the sibling relationship. His description emphasizes the negative emotions associated with sibling relationships and concludes that, although these feelings diminish as children mature, the rivalry persists into adulthood. Few of his remarks about sibling relationships address gender differences, as Freud described relationships from his own perspective as a male. Therefore, he was also a firm believer in the idea of the Oedipus complex, in which male children inherently feel sexual impulses toward their mother and subsequent jealously toward their father—which could extend to heightened competition with siblings as well.

Another theorist who addressed the issue of sibling relationships was Walter Toman. In 1961, Toman published the book Family Constellation: Theory and Practice of a Psychological Game. The book suggests that birth order, gender, and spacing are significant factors in the development of personality and strongly influence the nature of personal relationships both within and outside the family of origin. Toman details eight sibling positions, such as oldest brother of brothers, youngest sister of brothers, and so on. While the generalizations presented in Toman’s work have significance as a basis of comparison, there are too many intervening variables and complexities in family life to use birth order theories as complete explanations for sibling relationships and family roles. Birth order, gender, and spacing are several of the many significant factors that shape the connections between siblings.

Sibling relationships play an important role in each child’s development. Since the works of Freud and Toman were published, researchers have expanded their studies of sibling rivalry to include the broader context of the family. There is growing evidence that the emotional climate of the family is directly related to the quality of the relationship of siblings. The parental relationship, factors of vulnerability in specific children, parental expectations, and family constellation variables each contribute to the development and intensity of sibling rivalry between brothers and sisters in a given family.

Bibliography

"Adoption and Sibling Rivalry." HealthyChildren.org. Amer. Academy of Pediatrics, 6 Jan. 2015. Web. 13 Feb. 2015.

Berk, Laura E. Child Development. 9th ed. Boston: Pearson Education, 2013. Print.

Boer, Frits, and Judy Dunn, eds. Children’s Sibling Relationships: Developmental and Clinical Issues. Hillsdale: Erlbaum, 1992. Print.

Colt, George Howe. "Sibling Rivalry: One Long Food Fight." New York Times. New York Times, 24 Nov. 2012. Web. 13 Feb. 2015.

Goldenthal, Peter. Beyond Sibling Rivalry: How to Help Your Children Become Cooperative, Caring, and Compassionate. New York: Holt, 2000. Print.

Greydanus, Donald E., Dilip R. Patel, and Helen D. Pratt, eds. Behavioral Pediatrics. 2 vols. 3rd ed. New York: Nova Biomedical, 2009. Print.

Kramer, Laurie, and Chad Radey. “Improving Sibling Relationships Among Young Children: A Social Skills Training Model.” Family Relations 46.3 (1997): 237–46. Print.

Leder, Jane Mersky. Brothers and Sisters: How They Shape Our Lives. New York: Ballantine, 1994. Print.

Mendelson, Morton J. Becoming a Brother: A Child Learns About Life, Family, and Self. Cambridge: MIT, 1990. Print.

Neifert, Marianne E. Dr. Mom’s Parenting Guide: Commonsense Guidance for the Life of Your Child. New York: Dutton, 1996. Print.

Norton, Amy. "Sibling Bullying Can Lead to Depression, Anxiety in Victims. U.S. News & World Report. U.S. News & World Report, 17 June 2013. Web. 13 Feb. 2015.

Pendley, Jennifer Shroff. "Sibling Rivalry." KidsHealth. Nemours Foundation, Aug. 2012. Web. 13 Feb. 2015.

Sulloway, Frank J. Born to Rebel: Birth Order, Family Dynamics, and Creative Lives. New York: Random, 1997. Print.

Toohey, Peter. "Sibling Rivalry, a History." Atlantic. Atlantic Monthly, 30 Nov. 2014. Web. 13 Feb. 2015.

Ziegahn, Suzen J. The Stepparent’s Survival Guide: A Workbook for Creating a Happy Blended Family. Oakland: New Harbinger, 2003. Print.