DysgeusiaDysgeusia (/dsu/ or /dsjuzi/) or parageusia is a distortion of the sense of taste. Dysgeusia is also often associated with ageusia, which is the complete lack of taste, and hypogeusia, which is the decrease in taste sensitivity. An alteration in taste or smell may be a secondary process in various disease states, or it may be the primary symptom. The distortion in the sense of taste is the only symptom, and diagnosis is usually complicated since the sense of taste is tied together with other sensory systems. Common causes of dysgeusia include chemotherapy, asthma treatment with albuterol, and zinc deficiency. Different drugs could also be responsible for altering taste and resulting in dysgeusia. Due to the variety of causes of dysgeusia, there are many possible treatments that are effective in alleviating or terminating the symptoms of dysgeusia. These include artificial saliva, pilocarpine, zinc supplementation, alterations in drug therapy, and alpha lipoic acid.

BackgroundThe sense of taste is based on the detection of chemicals by specialized taste cells in the mouth. The mouth, throat, larynx, and esophagus all have taste buds, which are replaced every ten days. Each taste bud contains receptor cells. Afferent nerves make contact with the receptor cells at the base of the taste bud.[3] A single taste bud is innervated by several afferent nerves, while a single efferent fiber innervates several taste buds.Fungiform papillae are present on the anterior portion of the tongue while circumvallate papillae and foliate papillae are found on the posterior portion of the tongue. The salivary glands are responsible for keeping the taste buds moist with saliva.A single taste bud is composed of four different types of cells, and each taste bud has at least 30 to 80 cells. Type I cells are thinly shaped, usually in the periphery of other cells. They also contain high amounts of chromatin. Type II cells have prominent nuclei and nucleoli with much less chromatin than Type I cells. Type III cells have multiple mitochondria and large vesicles. Type I, II, and III cells also contain synapses. Type IV cells are normally rooted at the posterior end of the taste bud. Every cell in the taste bud forms microvilli at the ends.In humans, the sense of taste is conveyed via three of the twelve cranial nerves. The chorda tympani is responsible for taste sensations from the anterior two thirds of the tongue, the glossopharyngeal nerve is responsible for taste sensations from the posterior one third of the tongue while a branch of the vagus nerve carries some taste sensations from the back of the oral cavity.

DiagnosisIn general, gustatory disorders are challenging to diagnose and evaluate. Because gustatory functions are tied to the sense of smell, the somatosensory system, and the perception of pain (such as in tasting spicy foods), it is difficult to examine sensations mediated through an individual system. In addition, gustatory dysfunction is rare when compared to olfactory disorders.Diagnosis of dysgeusia begins with the patient being questioned about salivation, swallowing, chewing, oral pain, previous ear infections (possibly indicated by hearing or balance problems), oral hygiene, and stomach problems. The initial history assessment also considers the possibility of accompanying diseases such as diabetes mellitus, hypothyroidism, or cancer.[10] A clinical examination is conducted and includes an inspection of the tongue and the oral cavity. Furthermore, the ear canal is inspected, as lesions of the chorda tympani have a predilection for this site.Gustatory testingIn order to further classify the extent of dysgeusia and clinically measure the sense of taste, gustatory testing may be performed. Gustatory testing is performed either as a whole-mouth procedure or as a regional test. In both techniques, natural or electrical stimuli can be used. In regional testing, 20 to 50 L of liquid stimulus is presented to the anterior and posterior tongue using a pipette, soaked filter-paper disks, or cotton swabs. In whole mouth testing, small quantities (2-10 mL) of solution are administered, and the patient is asked to swish the solution around in the mouth.

Threshold tests for sucrose (sweet), citric acid (sour), sodium chloride (salty), and quinine or caffeine (bitter) are frequently performed with natural stimuli. One of the most frequently used techniques is the "three-drop test."[11] In this test, three drops of liquid are presented to the subject. One of the drops is of the taste stimulus, and the other two drops are pure water.[11] Threshold is defined as the concentration at which the patient identifies the taste correctly three times in a row.Suprathreshold tests, which provide intensities of taste stimuli above threshold levels, are used to assess the patient's ability to differentiate between different intensities of taste and to estimate the magnitude of suprathreshold loss of taste. From these tests, ratings of pleasantness can be obtained using either the direct scaling or magnitude matching method and may be of value in the diagnosis of dysgeusia. Direct scaling tests show the ability to discriminate among different intensities of stimuli and whether a stimulus of one quality (sweet) is stronger or weaker than a stimulus of another quality (sour). Direct scaling cannot be used to determine if a taste stimulus is being perceived at abnormal levels. In this case, magnitude matching is used, in which a patient is asked to rate the intensities of taste stimuli and stimuli of another sensory system, such as the loudness of a tone, on a similar scale. For example, the Connecticut Chemosensory Clinical Research Center asks patients to rate the intensities of NaCl, sucrose, citric acid and quinine-HCl stimuli, and the loudness of 1000 Hz tones. Assuming normal hearing, the results of this cross-sensory test show the relative strength of the sense of taste in relation to the loudness of the auditory stimulus. Although many of the tests are based on ratings using the direct scaling method, some tests do use the magnitude-matching procedure.Other tests include identification or discrimination of common taste substances. Topical anesthesia of the tongue has been reported to be of use in the diagnosis of dysgeusia as well, since it has been shown to relieve the symptoms of dysgeusia temporarily.[9] In addition to techniques based on the administration of chemicals to the tongue, electrogustometry is frequently used. It is based on the induction of gustatory sensations by means of an anodal electrical direct current. Patients usually report sour or metallic sensations similar to those associated with touching both poles of a live battery to the tongue.[13] Although electrogustometry is widely used, there seems to be a poor correlation between electrically and chemically induced sensations.Diagnostic toolsCertain diagnostic tools can also be used to help determine the extent of dysgeusia. Electrophysiological tests and simple reflex tests may be applied to identify abnormalities in the nerve-to-brainstem pathways. For example, the blink reflex may be used to evaluate the integrity of the trigeminal nervepontine brainstemfacial nerve pathway, which may play a role in gustatory function.Structural imaging is routinely used to investigate lesions in the taste pathway. Magnetic resonance imaging allows direct visualization of the cranial nerves. Furthermore, it provides significant information about the type and cause of a lesion.Analysis of mucosal blood flow in the oral cavity in combination with the assessment of autonomous cardiovascular factors appears to be useful in the diagnosis of autonomic nervous system disorders in burning mouth syndrome and in patients with inborn disorders, both of which are associated with gustatory dysfunction. Cell cultures may also be used when fungal or bacterial infections are suspected.In addition, the analysis of saliva should be performed, as it constitutes the environment of taste receptors, including transport of tastes to the receptor and protection of the taste receptor. Typical clinical investigations involve sialometry and sialochemistry. Studies have shown that electron micrographs of taste receptors obtained from saliva samples indicate pathological changes in the taste buds of patients with dysgeusia and other gustatory disorders.CausesChemotherapyA major cause of dysgeusia is chemotherapy for cancer. Chemotherapy often induces damage to the oral cavity, resulting in oral mucositis, oral infection, and salivary gland dysfunction. Oral mucositis consists of inflammation of the mouth, along with sores and ulcers in the tissues. Healthy individuals normally have a diverse range of microbial organisms residing in their oral cavities; however, chemotherapy can permit these typically non-pathogenic agents to cause serious infection, which may result in a decrease in saliva. In addition, patients who undergo radiation therapy also lose salivary tissues. Saliva is an important component of the taste mechanism. Saliva both interacts with and protects the taste receptors in the mouth. Saliva mediates sour and sweet tastes through bicarbonate ions and glutamate, respectively. The salt taste is induced when sodium chloride levels surpass the concentration in the saliva. It has been reported that 50% of chemotherapy patients have suffered from either dysgeusia or another form of taste impairment.Examples of chemotherapy treatments that can lead to dysgeusia are cyclophosphamide, cisplatin, and etoposide. The exact mechanism of chemotherapy-induced dysgeusia is unknown.Taste budsDistortions in the taste buds may give rise to dysgeusia. In one study conducted by Masahide Yasuda and Hitoshi Tomita from Nihon University of Japan, it has been observed that patients suffering from this taste disorder have fewer microvilli than normal. In addition, the nucleus and cytoplasm of the taste bud cells have been reduced. Based on their findings, dygeusia results from loss of microvilli and the reduction of Type III intracellular vesicles, all of which could potentially interfere with the gustatory pathway.Zinc deficiencyAnother primary cause of dysgeusia is zinc deficiency. While the exact role of zinc in dysgeusia is unknown, it has been cited that zinc is partly responsible for the repair and production of taste buds. Zinc somehow directly or indirectly interacts with carbonic anhydrase VI, influencing the concentration of gustin, which is linked to the production of taste buds. It has also been reported that patients treated with zinc experience an elevation in calcium concentration in the saliva. In order to work properly, taste buds rely on calcium receptors. Zinc is an important cofactor for alkaline phosphatase, the most abundant enzyme in taste bud membranes; it is also a component of a parotid salivary protein important to the development and maintenance of normal taste buds.DrugsThere are also a wide variety of drugs that can trigger dysgeusia, including zopiclone, H1-antihistamines, such as azelastine and emedastine. Approximately 250 drugs affect taste. The sodium channels linked to taste receptors can be inhibited by amiloride, and the creation of new taste buds and saliva can be impeded by antiproliferative drugs. Saliva can have traces of the drug, giving rise to a metallic flavor in the mouth; examples include lithium carbonate and tetracyclines. Drugs containing sulfhydryl groups, including penicillamine and captopril, may react with zinc and cause deficiency. Metronidazole and chlorhexidine have been found to interact with metal ions that associate with the cell membrane. Drugs that prevent the production of angiotensin II by inhibiting angiotensin converting enzyme, eprosartan for example, have been linked to dysgeusia. There are few case reports claiming calcium channel blockers like Amlodipine also cause dysguesia by blocking calcium sensitive taste buds.

DiplopiaWhat Causes Double Vision?Opening your eyes and seeing a single, clear image is something you probably take for granted. But that seemingly automatic process depends on the orchestration of multiple areas of the vision system. They all need to work together seamlessly:The cornea is the clear window into the eye. It does most of the focusing of incoming light.The lens is behind the pupil. It also helps focus light onto the retina.Muscles of the eye -- extraocular muscles -- rotate the eye.Nerves carry visual information from the eyes to the brain.The brain is where several areas process visual information from the eyes.Problems with any part of the vision system can lead to double vision.Cornea problems. Problems with the cornea often cause double vision in one eye only. Covering the affected eye makes the double vision go away. The abnormal surface of the eye distorts incoming light, causing double vision. Damage can happen in several ways:Infections of the cornea, such as herpes zoster, or shingles, can distort the cornea.Corneal scars can alter the cornea, creating unequal visual images.Dryness of the cornea can create double vision.Lens problems. Cataracts are the most common problem with the lens that causes double vision. If cataracts are present in both eyes, images from both eyes will be distorted. Cataracts are often correctable with minor surgery.Muscle problems. If a muscle in one eye is weak, that eye can't move smoothly with the healthy eye. Gazing in directions controlled by the weak muscle causes double vision. Muscle problems can result from several causes:Myasthenia gravis is an autoimmune illness that blocks the stimulation of muscles by nerves inside the head. The earliest signs are often double vision and drooping eyelids, or ptosis.Graves' disease is a thyroid condition that affects the muscles of the eyes. Graves' disease commonly causes vertical diplopia. With vertical diplopia, one image is on top of the other.

Diplopia, commonly known as double vision, is the simultaneous perception of two images of a single object that may be displaced horizontally, vertically, diagonally (i.e., both vertically and horizontally), or rotationally in relation to each other.[1] It is usually the result of impaired function of the extraocular muscles (EOMs), where both eyes are still functional but they cannot converge to target the desired object.[1] Problems with EOMs may be due to mechanical problems, disorders of the neuromuscular junction, disorders of the cranial nerves (III, IV, and VI) that stimulate the muscles, and occasionally disorders involving the supranuclear oculomotor pathways or ingestion of toxins.Diplopia can be one of the first signs of a systemic disease, particularly to a muscular or neurological process,[3] and it may disrupt a persons balance, movement, and/or reading abilities.

ClassificationBinocularBinocular diplopia is double vision arising as a result of strabismus (in layman's terms cross-eyed), the misalignment of the two eyes relative to each other either esotropia (inward) or exotropia (outward). In such a case while the fovea of one eye is directed at the object of regard, the fovea of the other is directed elsewhere, and the image of the object of regard falls on an extra-foveal area of the retina.The brain calculates the 'visual direction' of an object based upon the position of its image relative to the fovea. Images falling on the fovea are seen as being directly ahead, while those falling on retina outside the fovea may be seen as above, below, right or left of straight ahead depending upon the area of retina stimulated. Thus, when the eyes are misaligned, the brain will perceive two images of one target object, as the target object simultaneously stimulates different, non-corresponding, retinal areas in either eye, thus producing double vision.

This correlation of particular areas of the retina in one eye with the same areas in the other is known as retinal correspondence. This relationship also gives rise to an associated phenomenon of binocular diplopia, although one that is rarely noted by those experiencing diplopia: Because the fovea of one eye corresponds to the fovea of the other, images falling on the two foveas are 'projected' to the same point in space. Thus, when the eyes are misaligned, two different objects will be perceived as superimposed in the same space. This phenomenon is known as 'visual confusion'.The brain naturally guards against double vision. In an attempt to avoid double vision, the brain can sometimes ignore the image from one eye; a process known as suppression. The ability to suppress is to be found particularly in childhood when the brain is still developing. Thus, those with childhood strabismus almost never complain of diplopia while adults who develop strabismus almost always do. While this ability to suppress might seem an entirely positive adaptation to strabismus, in the developing child this can prevent the proper development of vision in the affected eye resulting in amblyopia. Some adults are also able to suppress their diplopia, but their suppression is rarely as deep or as effective and takes longer to establish, and thus they are not at risk of permanently compromising their vision. Hence, in some cases diplopia disappears without medical intervention, but in other cases the cause of the double vision may still be present.Certain persons with diplopia who cannot achieve fusion and yet do not suppress may display a certain type of spasm-like irregular movement of the eyes in the vicinity of the fixation point (see: Horror fusionis).

MonocularMore rarely, diplopia can also occur when viewing with only one eye; this is called monocular diplopia, or, where the patient perceives more than two images, monocular polyopia. In this case, the differential diagnosis of multiple image perception includes the consideration of such conditions as corneal surface keratoconus, subluxation of the lens, a structural defect within the eye, a lesion in the anterior visual cortex or non-organic conditions.

TemporaryTemporary diplopia can be caused by alcohol intoxication or head injuries, such as concussion (if temporary double vision does not resolve quickly, one should see an optometrist or ophthalmologist immediately). It can also be a side effect of benzodiazepines or opioids, particularly if used in larger doses for recreation, the anti-epileptic drugs Phenytoin and Zonisamide, and the anti-convulsant drug Lamotrigine, as well as the hypnotic drug Zolpidem and the dissociative drugs Ketamine and Dextromethorphan. Temporary diplopia can also be caused by tired and/or strained eye muscles or voluntarily. If diplopia appears with other symptoms such as fatigue and acute or chronic pain, the patient should see an optometrist immediately.VoluntarySome people are able to consciously uncouple their eyes, either by over focusing closely (i.e. going cross eyed) or unfocusing. Also, while looking at one object behind another object, the foremost object's image is doubled (for example, placing one's finger in front of one's face while reading text on a computer monitor). In this sense double vision is neither dangerous nor harmful, and may even be enjoyable. It makes viewing stereograms possible.CausesDiplopia has a diverse range of ophthalmologic, infectious, autoimmune, neurological, and neoplastic causes.AbscessAnisometropiaBotulismBrain tumorCancerDamaged third, fourth, or sixth cranial nerves, which control eye movements.DiabetesDrunkennessFluoroquinolone antibiotics[6]Graves diseaseGuillain-Barr syndromeKeratoconusLyme DiseaseMigraine headachesMultiple sclerosisMyasthenia gravisOpioidsOrbital myositisTraumaSalicylismSinusitisStrabismusWernicke's syndromeTreatmentThe appropriate treatment for binocular diplopia will depend upon the cause of the condition producing the symptoms. Efforts must first be made to identify and treat the underlying cause of the problem. Treatment options include eye exercises, wearing an eye patch on alternative eyes, prism correction, and in more extreme situations, surgery or botulinum toxin.If diplopia turns out to be intractable, it can be managed as last resort by obscuring part of the patient's field of view. This approach is outlined in the article on diplopia occurring in association with a condition called horror fusionis.

Male reproductive systemScrotumThe scrotum is a sac-like organ made of skin and muscles that houses the testes. It is located inferior to the penis in the pubic region. The scrotum is made up of 2 side-by-side pouches with a testis located in each pouch. The smooth muscles that make up the scrotum allow it to regulate the distance between the testes and the rest of the body. When the testes become too warm to support spermatogenesis, the scrotum relaxes to move the testes away from the bodys heat. Conversely, the scrotum contracts to move the testes closer to the bodys core heat when temperatures drop below the ideal range for spermatogenesis.

TestesThe 2 testes, also known as testicles, are the male gonads responsible for the production of sperm and testosterone. The testes are ellipsoid glandular organs around 1.5 to 2 inches long and an inch in diameter. Each testis is found inside its own pouch on one side of the scrotum and is connected to the abdomen by a spermatic cord and cremaster muscle. The cremaster muscles contract and relax along with the scrotum to regulate the temperature of the testes. The inside of the testes is divided into small compartments known as lobules. Each lobule contains a section of seminiferous tubule lined with epithelial cells. These epithelial cells contain many stem cells that divide and form sperm cells through the process of spermatogenesis.EpididymisThe epididymis is a sperm storage area that wraps around the superior and posterior edge of the testes. The epididymis is made up of several feet of long, thin tubules that are tightly coiled into a small mass. Sperm produced in the testes moves into the epididymis to mature before being passed on through the male reproductive organs. The length of the epididymis delays the release of the sperm and allows them time to mature.

Spermatic Cords and Ductus DeferensWithin the scrotum, a pair of spermatic cords connects the testes to the abdominal cavity. The spermatic cords contain the ductus deferens along with nerves, veins, arteries, and lymphatic vessels that support the function of the testes.The ductus deferens, also known as the vas deferens, is a muscular tube that carries sperm superiorly from the epididymis into the abdominal cavity to the ejaculatory duct. The ductus deferens is wider in diameter than the epididymis and uses its internal space to store mature sperm. The smooth muscles of the walls of the ductus deferens are used to move sperm towards the ejaculatory duct through peristalsis.Seminal VesiclesThe seminal vesicles are a pair of lumpy exocrine glands that store and produce some of the liquid portion of semen. The seminal vesicles are about 2 inches in length and located posterior to the urinary bladder and anterior to the rectum. The liquid produced by the seminal vesicles contains proteins and mucus and has an alkaline pH to help sperm survive in the acidic environment of the vagina. The liquid also contains fructose to feed sperm cells so that they survive long enough to fertilize the oocyte.Ejaculatory DuctThe ductus deferens passes through the prostate and joins with the urethra at a structure known as the ejaculatory duct. The ejaculatory duct contains the ducts from the seminal vesicles as well. During ejaculation, the ejaculatory duct opens and expels sperm and the secretions from the seminal vesicles into the urethra.UrethraSemen passes from the ejaculatory duct to the exterior of the body via the urethra, an 8 to 10 inch long muscular tube. The urethra passes through the prostate and ends at the external urethral orifice located at the tip of the penis. Urine exiting the body from the urinary bladder also passes through the urethra.

ProstateThe prostate is a walnut-sized exocrine gland that borders the inferior end of the urinary bladder and surrounds the urethra. The prostate produces a large portion of the fluid that makes up semen. This fluid is milky white in color and contains enzymes, proteins, and other chemicals to support and protect sperm during ejaculation. The prostate also contains smooth muscle tissue that can constrict to prevent the flow of urine or semen.Cowpers GlandsThe Cowpers glands, also known as the bulbourethral glands, are a pair of pea-sized exocrine glands located inferior to the prostate and anterior to the anus. The Cowpers glands secrete a thin alkaline fluid into the urethra that lubricates the urethra and neutralizes acid from urine remaining in the urethra after urination. This fluid enters the urethra during sexual arousal prior to ejaculation to prepare the urethra for the flow of semen.PenisThe penis is the male external sexual organ located superior to the scrotum and inferior to the umbilicus. The penis is roughly cylindrical in shape and contains the urethra and the external opening of the urethra. Large pockets of erectile tissue in the penis allow it to fill with blood and become erect. The erection of the penis causes it to increase in size and become turgid. The function of the penis is to deliver semen into the vagina during sexual intercourse. In addition to its reproductive function, the penis also allows for the excretion of urine through the urethra to the exterior of the body.SemenSemen is the fluid produced by males for sexual reproduction and is ejaculated out of the body during sexual intercourse. Semen contains sperm, the male reproductive gametes, along with a number of chemicals suspended in a liquid medium. The chemical composition of semen gives it a thick, sticky consistency and a slightly alkaline pH. These traits help semen to support reproduction by helping sperm to remain within the vagina after intercourse and to neutralize the acidic environment of the vagina. In healthy adult males, semen contains around 100 million sperm cells per milliliter. These sperm cells fertilize oocytes inside the female fallopian tubes.SpermatogenesisSpermatogenesis is the process of producing sperm and takes place in the testes and epididymis of adult males. Prior to puberty, there is no spermatogenesis due to the lack of hormonal triggers. At puberty, spermatogenesis begins when luteinizing hormone (LH) and follicle stimulating hormone (FSH) are produced. LH triggers the production of testosterone by the testes while FSH triggers the maturation of germ cells. Testosterone stimulates stem cells in the testes known as spermatogonium to undergo the process of developing into spermatocytes. Each diploid spermatocyte goes through the process of meiosis I and splits into 2 haploid secondary spermatocytes. The secondary spermatocytes go through meiosis II to form 4 haploid spermatid cells. The spermatid cells then go through a process known as spermiogenesis where they grow a flagellum and develop the structures of the sperm head. After spermiogenesis, the cell is finally a sperm cell, or spermatozoa. The spermatozoa are released into the epididymis where they complete their maturation and become able to move on their own.FertilizationFertilization is the process by which a sperm combines with an oocyte, or egg cell, to produce a fertilized zygote. The sperm released during ejaculation must first swim through the vagina and uterus and into the fallopian tubes where they may find an oocyte. After encountering the oocyte, sperm next have to penetrate the outer corona radiata and zona pellucida layers of the oocyte. Sperm contain enzymes in the acrosome region of the head that allow them to penetrate these layers. After penetrating the interior of the oocyte, the nuclei of these haploid cells fuse to form a diploid cell known as a zygote. The zygote cell begins cell division to form an embryo.