Holistic Treatment to get rid of Vertigo and Dizziness

Vertigo And Dizziness Program

You will learn: How to strengthen and loosen up the tongue. This is more important than you might imagine! The 4 most powerful exercises to establish whole-body balance. How to quickly straighten your head so that the fluid in your inner ear can regulate your balance. How to loosen up those stiff jaw muscles that are contributing to vertigo symptoms. How to relieve tension line between your shoulders and your jaw. Each of these muscle groups contributes to your dizziness, and Im going to teach you exactly to how deal with them all! How to use powerful breathing exercise to quickly eliminate dizziness, even in the midst of your worst vertigo attack. A simple, little-known breathing exercise that will change the way you breathe every day, relieving the tension that grips your muscles and causes vertigo symptoms. Continue reading...

Vertigo And Dizziness Program Overview


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Syncope And Dizziness

It is uncommon for dizziness to be caused by cardiac disease. However, loss of consciousness (syncope) or the feeling of impending loss of consciousness (presyncope) may be cardiac in origin. The causes can be broadly classified into three groups Some of the drugs which may cause palpitations may also produce syncope or presyncope (Table 3.2). Vasodilator drugs (e.g. alpha-biockers) can cause symptomatic postural hypotension. Beta-blockers, verapamil, diltiazem and digoxin can aggravate or cause sinoatrial disease or atrioventricular block. Other cardiac and non-cardiac medications can directly (e.g. tricyclic antidepressants) or indirectly (e.g. diuretics causing hypokalemia) provoke ventricular arrhythmias in vulnerable patients.

Nonvestibular Vertigo

Unsteady Gait

Episodic or persistent nonvestibular vertigo often manifests itself as staggering, unsteady gait, and loss of balance. The possible causes include disturbances of the oculomotor apparatus, cerebellum, or spinal cord peripheral neuropathy intoxication anxiety (phobic attacks of vertigo) hyperventilation metabolic disorders and cardiovascular disease. Rotatory vertigo Rotatory vertigo Nonvestibular vertigo (unsteady posture gait nondirectional vertigo) Benign peripheral paroxysmal positional vertigo Benign peripheral paroxysmal positional vertigo

High resolution linkage disequilibrium mapping of QTLs

High resolution mapping in future will rely increasingly not on the detection of linkage, but on the occurrence of linkage disequilibrium, that is non-random associations between pairs of loci detectable at the population level rather than the family or pedigree level. There is insufficient opportunity for enough recombination to accumulate over the course of a two or three generation pedigree to map QTLs with anything but very coarse precision, generally no better than about 20 cM resolution. However, appropriately designed resources can exploit the combined historical accumulation of recombination by utilizing linkage disequilibrium to map genes of interest to much higher resolution and therefore assist in their identification and use. Cardon and Abecasis (2003) have described preliminary progress in the human HapMap project which eventually aims to use many thousands of closely spaced single nucleotide polymorphism (SNP) markers to precisely map and identify loci affecting complex...

Dizziness and Vertigo

The term vertigo refers to the sensation of spinning, which, when severe, may be accompanied by nausea and vomiting. There are many causes of vertigo. In MS the problem usually results from an irritation of the brain stem structures that help to maintain balance by coordinating the eyes, arms, and legs. The inner ears also play a major role in balance, and disturbances in the conduction of input to the brain from the inner ear may be very distressing. Dizziness and the sensation of lightheadedness are less severe than vertigo, but nonetheless they cause discomfort. Obviously, other diseases that involve these structures produce similar symptoms, and it should not be assumed that they are necessarily due to MS. Antihistamines, including diphenhydramine (Benadryl ), meclizine (Antivert ), and dimenhydrinate (Dramamine ), frequently provide relief when vertigo or sensations of dizziness are relatively mild. Niacin (a component of vitamin B complex) occasionally is used to dilate blood...

Benign Paroxysmal Vertigo

Benign paroxysmal vertigo is reflected by the recurrence of events of brief dysequilibrium in young children. When the attacks occur, the child appears frightened and off balance, often reaching out to steady himself. The events may be associated with nystagmus, diaphoresis, nausea, and vomiting. These attacks occur in toddlers and young children but typically resolve by age 5 years. Neurologic examination, development, and EEG are normal. A later association with migraine has been reported (21).

Disturbances of Hearing and Balance Vertigo

Lesions of the vestibulocochlear n. can impair hearing, balance, or both. A lesion of its cochlear portion produces sensorineural hearing loss (impairment of sound perception), which must always be differentiated from conductive hearing loss (impairment of sound conduction, usually due to blockage of the external auditory canal by cerumen, or to a disease process in the middle ear). A lesion of the vestibular portion causes disequilibrium and vertigo. Vestibular vertigo usually occurs in a particular direction and is accompanied by autonomic symptoms and nystagmus. Common vestibular disorders causing vertigo include vestibular neuritis and benign paroxysmal positioning vertigo. A vestibular lesion, however, is only one possible cause of vertigo many other disorders must be included in the differential diagnosis.

Disequilibrium and Vertigo

The vestibular organ (semicircular canals, saccule, and utricle) plays a central role in the regulation of balance. Disturbances of the vestibular apparatus (composed of the vestibular organ, the vestibulocochlear n., and the vestibular nuclei of the brainstem) cause dysequil-ibrium, the main symptom of which is vertigo. It must be emphasized, however, that vestibular disturbances are just one cause of vertigo (see below) and not even the most common one. Disturbances of the regulation of equilibrium. Vertigo arises if individual informational and or control components of the regulatory system are lost (see below), if the information coming through different sensory channels seems to be incompatible (so-called multisensory mismatch, e. g., in seasickness), or the sensory input is highly unusual (e. g., uncommon visual input from a great height). So many different structures play a role in the maintenance of equilibrium and their interactions are so complex, that the causes of vertigo...

Characteristics of Intracanalicular Acoustic Neuromas

An intracanalicular acoustic neuroma is < 1 cm in length and appears rounded in the early stages. Upon filling the internal auditory canal (IAC), it assumes an oblong shape. At diagnosis, three variations are encountered, depending on the extent of involvement of the IAC (1) medial IAC location near the porus acousticus, (2) lateral IAC involvement near the fundus, and (3) involvement of the entire IAC. True intracanalicular tumors involve only the IAC, although many tumors can be considered primarily intracanalicular with minimal cerebellopontine angle extension, and are readily accessible by surgical approaches to the IAC. It should be noted that whereas 90 of intracanalicular lesions are indeed acoustic neuromas, patients should be counseled regarding the possibility that a facial neuroma may be radiologically indistinguishable from an acoustic neuroma.2 Alternative management schemes in the event of the presence of a facial neuroma should be discussed preoperatively with the...

Use of linkage disequilibrium for gene mapping

Two genes may be found in linkage disequilibrium because they are physically close and recombination events do not occur frequently between them, thus linkage disequilibrium analyses have been used in gene mapping studies. Experimental approaches that make use of linkage disequilibrium have been successful in strengthening traditionally performed linkage analyses, particularly those involving genes with few alleles. Certain genes of interest for their role in a particular disease may not be highly polymorphic in a population, therefore the number of informative crosses available for examination may be limited. In addition to close physical linkage, there are other reasons why two genes may be found in linkage disequilibrium. Two populations with distinct traits may have merged recently. Associations between alleles or traits may be apparent because insufficient time has passed for the genes to segregate randomly. Alternatively, there may be functional interactions between the products...

Impact of linkage disequilibrium on studies of the HLA complex

Regardless of the basis for linkage disequilibrium, it has an important impact upon analyses of HLA antigens in functional and disease association studies. A historical review of the HLA antigens found to be associated with certain diseases illustrates this point. As new loci within the HLA complex were identified, associations with allelic variants of these new loci in linkage disequilibrium were shown to be stronger than previously observed associations. The number of genes mapping to the HLA complex continues to increase. Due to linkage disequilibrium, functional associations with allelic variants of the newly defined loci may be stronger than those observed with previously characterized loci. While the HLA gene complex provides the best known examples of linkage disequilibrium, this phenomenon is not limited to HLA. Linkage disequilibrium may also be a consideration when examining other gene complexes encoding immunologically relevant molecules. For example, the immunoglobulin...

Disorders Causing Central Vertigo

Central vertigo is caused by disorders affecting the cerebellum and the brainstem. It can produce a strikingly different clinical picture from that of peripheral vertigo. The onset is usually gradual, the sensation less intense, and symptoms are not provoked by changes in position. Central vertigo is unlikely to be associated with nausea, vomiting, or diaphoresis. Unlike conditions causing peripheral vertigo, both tinnitus and hearing impairment are unlikely. Nystagmus is more likely to be vertical than horizontal or rotatory and may be present in the absence of vertigo. Oscillopsia is a common finding. Central vertigo tends to be accompanied by other signs of brainstem disease, such as ataxia, blurred vision, long tract signs, dysphagia, dysarthria, and diplopia.

Migraine Related Dizziness and Vertigo

Vertigo can be a symptom of an aura, an analogue or equivalent of the headache phase itself, or as an associated symptom to the migraine prodromes. Basilar migraine is a migraine headache in which the aura is associated with clinical manifestations similar to those of VBI. The International Headache Society's diagnostic criteria for basilar migraine9 are shown in I ble 223-5 These include vertigo, decreased hearing, tinnitus, bilateral long-tract signs, bilateral visual disturbances, dysarthria, diplopia, and decreased level of consciousness. Vertigo as an aura should develop over 5 to 20 min and should subside within 60 min. Vertigo as a symptom of a migraine aura may precede the headache or may occur in the absence of a headache. The headache is typically occipital in location, throbbing in character, and associated with nausea and vomiting.

TABLE 2237 Precipitants of Dizziness

Because of central adaptation, true vertigo is unlikely to be constant. Thus, constant symptoms are more likely to represent nonvertiginous dizziness and psychogenic complaints. A history of numerous chronic somatic complaints increases this possibility. When such a pattern emerges, it is prudent to obtain a psychiatric history and to ask about panic disorder and agoraphobia. However, the diagnosis of psychogenic symptomatology should only be entertained after other potential causes have been ruled out, and thus it is rarely if ever appropriate to entertain in the ED. Constant oscillopsia suggests a central neurologic diagnosis.

TABLE 2314 Causes of Vertigo

BENIGN POSITIONAL VERTIGO BPV is the most common form of peripheral vertigo. Generally, the patient will complain that the vertigo occurs with head movement, typically while turning over in bed or quickly turning the head to one side it usually lasts seconds to minutes. It is most often idiopathic in nature but is also common secondary to head trauma or viral infections. The peak age of onset is during the sixth decade in the idiopathic group, with a 2 1 female predominance, and in the fourth and fifth decades in the posttraumatic group, with no gender predominance. The pathophysiology of BPV is disputed, but it has been thought to result from lesions of the otolith organs of the inner ear or from deposits in the semicircular canals. BPV is by definition paroxysmal and positional and is reproducible using the Dix-Hallpike maneuver. The nystagmus elicited is usually but not always extinguishable. 3 LABYRINTHITIS Labyrinthitis, or vestibular neuronitis, is characterized by the acute...

Benign Paroxysmal Vertigo of Childhood

This is the most common of the migraine equivalents (116). Although affected preschool children are often referred to as having epilepsy, the characteristic history of anxious arrest of movement without loss of awareness and subjective vertigo or drunking makes the diagnosis easy. A related migraine equivalent, benign paroxysmal torticollis of infancy, has been discussed under Paroxysmal Disorders of Movement.

Hyperventilation Syndrome

Acute hypocalcemia often leads to dystonic contractions of the fingers, hands, wrist, and face, which may be confused with motor seizures. Because the manifestations of anxiety are less intense, hyperventilation syndrome may be more difficult to differentiate from epilepsy on clinical grounds alone. Nevertheless, a heightened level of suspicion usually allows the clinical diagnosis, which is helped by a history of flexion of both wrists.

Sources Of Linkage Disequilibrium

Given that some initial linkage disequilibrium is necessary before recombination can act as an evolutionary force in a random-mating population, it is important to understand what factors can create an initial disequilibrium. Many factors can create linkage disequilibrium, including Note that this list of factors that can generate linkage disequilibrium corresponds to the very same factors that are assumed not to occur in the simple Hardy-Weinberg model (Table 2.1). All of these factors will be considered in this book, but for now we focus only upon the first mutation. The impact of mutation is most easily seen by considering another measure of linkage disequilibrium known as the normalized linkage disequilibrium D', which is the linkage disequilibrium divided by its theoretical maximum absolute value. Because two-locus gamete frequencies cannot be negative or greater than the corresponding single-locus allele frequencies (equation 2.7), we have that

Some Implications Of Impact Of Evolutionary History Upon Disequilibrium

The impact of the past as measured by D0 upon the present in multilocus systems can be either a boon or a bane, depending upon the question being addressed. As a boon, multilocus studies inherently contain information about the past history of present-day genetic variation and its mutational origins. Parts of this history can often be inferred from multilocus (or multi-nucleotide-site) studies and hence give us a window into the past. For example, one important mutation in human genetics is the sickle cell mutation in the sixth codon of the autosomal locus that codes for the j chain of adult hemoglobin. We will look at the phenotypic and adaptive significance of this mutation later in this book. For now we focus on the linkage disequilibrium patterns of this relatively new mutation in the human gene pool with some genetic variation in surrounding loci. Figure 2.6 shows the genetic state of some of these surrounding loci on chromosomes that contain the j S allele. As will be detailed...

Haplotypes And Linkage Disequilibrium

When several alleles exist at independent polymorphic loci, the frequencies of expected combinations of alleles in the population is given by the product of the allele frequencies. For example, if locus A has two alleles, Ai and A2, with frequencies of 0.3 and 0.7, and locus B also has two alleles, B1 and B2, with frequencies of 0.6 and 0.4, then the expected frequencies of combinations of alleles are Ai Bi 0.18 (i.e., 0.3 x 0.6) A1 B2 0.12 A2 B1 0.42 and A2 B2 0.28. If these findings were observed in a population, then the markers would be referred to as being in linkage equilibrium. When markers on a chromosome are not randomly associated with each other, they are said to be in linkage disequilibrium. For example, a deletion that includes both the steroid 21-hydroxylase gene (CYP21) and the adjacent complement 4B gene is frequently seen on a haplotype that includes the HLA markers A3, B47, and DR7 (14). This haplotype is associated with congenital adrenal hyperplasia because of...

Linkage Disequilibrium Ld Mapping And Identical By Descent Ibd Mapping

When marker and QTL are very close together, or when the marker is within the DNA sequence of the gene itself, a situation may arise in which there is an excess of some haplotypes and a deficiency of others across the population as a whole. This condition, termed linkage disequilibrium (LD), can be uncovered by an association test, which compares average trait value of the different genotypes at a marker across the population as a whole. Finding marker QTL LD indicates that the marker involved is very close to the QTL. Linkage disequilibrium can be generated by the random accumulation of small changes in frequency of the various marker QTL haplotypes over many generations. Identical by descent (IBD) mapping is based on the assumption that the mutation that produced a specific positive or negative QTL allele was a unique event that took place in a single ancestor chromosome, and will hence be in association with the specific marker alleles found in the haplotype of the ancestor...

Genetic Drift And Disequilibrium

Just as drift causes changes in allele frequencies, it also changes multilocus gamete frequencies. Genetic drift tends to create linkage disequilibrium and associations between loci by chance alone. As we consider more and more loci simultaneously, we subdivide any finite gene pool into more and more gametic categories, thereby tending to make any one particular gamete type more rare. Sampling error is a strong force of evolutionary change for any gamete type that is rare in a gene pool, so in general genetic drift is a more powerful force for altering gamete frequencies at the multilocus level than at the single-locus level. The increased sensitivity of linkage disequilibrium to drift compared to allele frequencies is illustrated by a study of 34 X-linked microsatellite loci in the United Kingdom and in 10 regions in Scotland (Vitart et al. 2005) the urban region of Edinburgh and 9 rural regions. The rural regions had smaller populations sizes (but still in the tens of thousands or...

Linkage Disequilibrium And Multilocus Associations

As shown in Chapter 2, both past history as well as recurrent evolutionary forces influence the genetic parameter of linkage disequilibrium, D. The creation of disequilibrium is influenced by historical factors such as the exact haplotype background upon which a new mutation originated or historical admixture between two previously genetically differentiated subpopulations (Chapter 2). Recurrent processes such as the system of mating and the amount of recombination then influence the decay of linkage disequilibrium over time a decay that can be quite slow for closely linked genes or sites. This slow decay means that the signature of the historical events that initially created linkage disequilibrium is often apparent for many generations. For example, in Chapters 3 and 6 we saw that the current African American gene pool has been greatly shaped by historical admixture between previously differentiated European and African populations (see Figure 6.2). In human populations without...

Markers of Intrapopulation Disequilibrium

The founder populations most likely to have strong associations with noncausative markers are those that have experienced little or no subsequent gene flow with other populations after the founder event. Postfounder reproductive isolation allows the persistence of the linkage disequilibrium patterns, commonness of a phenotype of interest, and the genetic background homogeneity induced by the original founder or bottleneck event. Moreover, sampling individuals from a relatively isolated population makes it less likely to inadvertently sample individuals from more than one local deme in a subdivided population. Pooling individuals from genetically differentiated demes creates linkage disequilibrium in the total sample that is a function only of the allele frequency differences between demes and is independent of actual linkage relationships (equation 6.3). Disequilibrium that is independent of true linkage undercuts the fundamental biological premise of the marker association analysis...

Disease Of The Inner Earlabyrinthitis

Labyrinthitis is a suppurative (pus-forming) causing disease process arising from chronic otitis media. The cause of this disease includes trauma associated with concussion producing bleeding such as a crack in the cochlea and nasal skull fracture. The condition may be caused by cardiovascular diseases such as arteriosclerosis and certain allergies. (3) Vertigo. c. Treatment. Treatment for labyrinthitis should be confined to symptomatic treatment of the underlying cause, if that cause is known. Promethazine (Phenergan ) is used for motion sickness and thiethylperazine (Torecan ) is given for nausea and vomiting. The medical evacuation procedures should be done carefully. It may be dangerous aboard ship or aircraft.

Applications Of Linkage Disequilibrium And Association Mapping In Crop Plants

Abstract The investigations of patterns of linkage disequilibrium for designing association-mapping studies are fast becoming a method of interest for complex trait dissection and improvement practices in many crop plants. The methodology and its applications to crop improvement, to date are discussed.

Treatment Strategies in Patients with Acoustic Neuromas

When considering the management of a patient with an acoustic neuroma, several factors preside. The size of the tumor is of paramount importance. In the Cambridge series of 473 patients presenting between 1983 and 1995, 47 of tumors were large (more than 2.5 cm), 32 medium (1.5-2.5 cm) and 21 small (less than 1.5 cm). Large tumors may cause the life-threatening complications of symptomatic hydro-cephalus, and direct mass effect. We advocate initial insertion of a ventriculoperitoneal shunt, or, in suitable cases, a third ventriculostomy, to alleviate hydrocephalus. If mass symptoms are evident, early surgery to remove the tumor should be considered. The initial presentation of these tumors in this way is now rare. At presentation, most acoustic neuromas present with audiovestibular symptoms and do not constitute a threat to life at that time. A complete understanding of the natural history, surgical morbidity and success of radiosurgery is of importance in deciding the appropriate...

Results of Acoustic Neuroma Surgery

The objective of acoustic neuroma surgery is the total removal of the neoplasm with minimal morbidity and mortality. Objective recording of cranial nerve function, CSF leak rates, meningitis incidence and quality-of-life assessments can assess morbidity. Extent of tumor removal can be determined intraoperatively, and recurrence can be monitored with MRI scans. In the modern era, total tumor removal should be achieved. This was the case in 99.6 of patients with unilateral tumors in Cambridge. Recurrence of acoustic neuromas is exceptional, and has only been seen in two patients in our center between 1982 and 1998. In one of these cases (a patient with NF-2), the tumor was histologically malignant. We perform MRI scans 2 and 5 years post-operatively to ensure recurrence has not occurred. The mortality of surgery for acoustic neuromas has reduced dramatically over the course of this century. Whilst Cushing's overall operative mortality was 11.4 12 , mortality figures of around 20 were...

Benign positional vertigo

Benign positional vertigo is the most common cause of vertigo. Patients have brief episodes with positional change, typically when turning over in bed, getting out of bed, or bending over and straightening up. It is most common in older people. B. Diagnosis is by the Dix-Hallpike maneuver fatigable, torsional, vertical, paroxysmal positional nystagmus resulting from a rapid change from the sitting to the head-hanging position. Benign positional vertigo is caused by calcium within the posterior semicircular canal. IV. Acute unilateral vestibulopathy is characterized by acute onset of vertigo, nausea, and vomiting lasting for several days, not associated with auditory or neurologic symptoms. Most patients gradually improve over a few weeks, but older patients can have persistent symptoms for months. About half of patients report having had a recent viral upper respiratory tract infection.

Psychiatric Dizziness

Psychiatric dizziness is defined as dizziness that occurs in combination with other symptoms as part of a recognized psychiatric disorder or symptom complex that is not related to known vestibular disorders. Although such dizziness has been characterized as nonvertiginous dizziness in the past, it is now recognized that patients with certain psychiatric disorders can present with true vertigo as part of their presenting symptoms. Dizziness is the second most common symptom reported by patients with panic disorder. In addition, a large percentage of patients with dizziness meet the criteria for panic or mood disorder. A majority of patients with panic disorder have objective abnormalities on testing of vestibular function. The strongest correlation is with patients who suffer from agoraphobia. Such patients suffer from what is known as space and motion discomfort (SMD). SMD is defined as comprising uncomfortable symptoms such as dizziness, imbalance, and anxiety occurring in situations...

Linkage Disequilibrium

Two linked loci are said to be in linkage disequilibrium if specific combinations of alleles at the loci are seen together on chromosomes more often than expected by chance. For example, if die frequency of allele 1 at locus A (Al) is 0.7 in a population and the frequency of allele 1 at locus B (Bl) is 0.6, then the expected proportion of chromosomes bearing the combination Al Bl is given by the product of the frequencies of Al and Bl 0.7 X 0.6 0.42. If we examine a series of chromosomes in a population and find that Al and Bl are found on the same chromosome significandy more often or less often than expected (e.g., suppose the frequency of chromosomes containing both alleles is only 0.3)> then the two loci are in linkage disequilibrium. Through time, recombination between two loci tends to distribute alleles so that they are in linkage equilibrium. Because recombination is rare for very closely linked loci, such loci are more likely to exhibit linkage disequilibrium (Fig II-4-3)....

Multilocus models and linkage disequilibrium

If an allele at site 1 is drawn at random from the population, it will be an'A' with probability pA and an'a' with probability pa likewise with locus 2. Then by the rules of probability, if the allele frequencies at each locus are independent of one another, the probability of drawing a certain two-locus haplotype is just the product of the two individual allele frequencies. For example, assuming independence, the predicted frequency of the AB haplotype is simply PAPB. When two alleles are statistically independent of each other, they are said to be in linkage equilibrium. When individuals are sampled from a single population, it is normally the case that pairs of loci located on different chromosomes, or pairs that are far apart on the same chromosome, will be in linkage equilibrium. However, when loci are sufficiently close together, there is often statistical correlation between the alleles at each locus. This correlation is referred to as...

Complications In Linkage Disequilibrium And Genetic Maps In General

The human genome is a potential minefield of uncharted genetic events, hidden rearrangements, new mutations, and genetic heterogeneity. Failure to see linkage disequilibrium near a gene does not mean that the gene is far away. Two of the most plausible potential complications are the existence of more than one founder or the existence of a significant fraction of alleles in the population that have arisen by new mutations. For example, in the case of dominant lethal diseases (those in which, nominally, the affected individuals have no offspring), one must expect that most disease alleles will be new mutations. Multiple founders can occur in distinct geographical populations, and they can be tested for by subdividing the linkage disequilibrium analysis accordingly. However, our increasingly mobile population, at least in developed countries, will make such analyses increasingly difficult. Two other reasonable explanations for a failure to see linkage disequilibrium near a disease gene...

Vertigo And Bowel Surgery

Small Bowel Series Technique

There are two types of dumping syndrome early and late with respect to the time interval following a meal. The early dumping syndrome consists of postprandial sweating, flushing, palpitation, vomiting, diarrhea, weakness, and dizziness, often relieved by assuming a recumbent position. It is in part due to rapid emptying of the gastric remnant and can be seen with all types of gastric surgery that cause disruption or bypass of the normal pyloric sphincter mechanism and subsequent loss of the gastric reservoir function. Stomach size may also contribute to the development of the dumping syndrome. It is thought that symp-

Antiemetic and Antivertigo Drugs

Vertigo vestibular neuritis vomiting An antiemetic drug is used to treat or prevent nausea (unpleasant gastric sensation usually preceding vomiting) or vomiting (forceful expulsion of gastric contents through the mouth). An antivertigo drug is used to treat or prevent vertigo (a feeling of a spinning or rotationtype motion) that may occur with motion sickness, Meniere's disease of the ear, middle and inner ear surgery, and other disorders. Vomiting caused by drugs, radiation, and metabolic disorders usually occurs because of stimulation of the chemoreceptor trigger zone (CTZ), a group of nerve fibers located on the surface of the fourth ventricle of the brain. When these fibers are stimulated by chemicals, such as drugs or toxic substances, impulses are sent to the vomiting center located in the medulla. The vomiting center may also be directly stimulated by disorders such as gastrointestinal irritation, motion sickness, and vestibular neuritis (inflammation of the vestibular nerve).

Benign Paroxysmal Peripheral Vertigo

Benign paroxysmal peripheral vertigo (BPPV) is one of the most common causes of peripheral vertigo, accounting for as many as 17 to 22 percent of patients presenting to dizziness clinics.5 The incidence of BPPV has been estimated as being as high as 64 per 100,000 per year. 6 This estimate was derived from patients seen only by ear nose throat (ENT) specialists, omitting those seen only by primary care physicians. Thus, the incidence may be underestimated. BPPV is defined as a mechanical disorder of the inner ear causing transient vertigo (with autonomic symptoms) and associated nystagmus that is precipitated by certain head movements. The condition was first described by Barany in 1921, and most of the essential clinical features were described by Dix and Hallpike in 1952. 7 The most widely accepted hypothesis to explain BPPV is known as canalolithiasis. According to this hypothesis, BPPV is caused by inappropriate activation of the posterior semicircular canal (typically unilateral)...

Peripheral Vestibular Labyrinthine Vertigo p

There is usually an acute, severe rotatory vertigo directed away from side of the labyrinthine lesion, with a tendency to fall toward the side of the lesion, horizontal nystagmus away from the side of lesion, nausea, and vomiting. Peripheral vestibular vertigo may depend on position, being triggered, for example, when the patient turns over in bed or stands up (positional ver-58 tigo), or it may be independent of position (persistent vertigo). It may also occur in attacks as episodic vertigo. Positional vertigo. Benign, paroxysmal positional vertigo (BPPV) of peripheral origin is usually due to detached otoliths of the utricular macula floating in the posterior semicircular canal (canalolithiasis). With every bodily movement, the freely floating otoliths move within the canal, under the effect of gravity. An abnormal cupular deflection results, starting 1-5 seconds after movement and lasting up to 30 seconds. The Dix-Hallpike maneuver is a provocative test for BPPV the patient is...

Management of vertigo and vestibular disorders

Vestibular syndromes are commonly characterized by a combination of phenomena involving perceived vertigo, nystagmus, ataxia, and nausea.1 These four manifestations correlate with different aspects of vestibular function and emanate from different sites within the central nervous system. The vertigo itself results from a disturbance of cortical spatial orientation. Vertigo, dizziness and disequilibrium are common complaints of patients of all ages, particularly the elderly. As presenting symptoms, they occur in 5-10 of all patients seen by general practitioners and 10-20 of all patients seen by neurologists and otolaryngologists. The clinical spectrum of vertigo is broad, extending from vestibular rotatory vertigo with nausea and vomiting to presyncope light-headedness, from drug intoxication to hypoglycemic dizziness, from visual vertigo to phobias and panic attacks, and from motion sickness to height vertigo. Appropriate preventions and treatments differ for different types of...

Nonvestibular Dizziness

Balance and spatial orientation depend on three main systems the vestibular apparatus, vision, and proprioception (position sense from the spine and pressure sensors of the extremities). Dizziness may result from problems involving any one, or more, of these systems. Furthermore, disease processes of other bodily systems, such as circulation, respiration, cerebration (including anxiety), and endocrine function, may cause dizziness by affecting the former ones Numerous types of nonvertiginous dizziness may occur, and the more notable types will be discussed briefly. Again, emphasis should be placed on eliciting an accurate descriptive history from the patient. A patient may be lightheaded, feel vaguely disoriented, have visual blurring, become faint, lose consciousness (experience syncope), or have disequilibrium. Certain positions or activities might bring on the symptoms. Anxiety, with hyperventilation, may be present. Postural changes, moving the neck, or using the arms may be...

Coca Leaves For Vertigo

Coca plants are the only natural source of the alkaloid cocaine and related compounds. For several thousand years, the leaves of the coca plant have been used by South American Indians as a mild stimulant, a remedy for medical problems, and for ritualistic or religious purposes. Coca chewing reduces hunger and increases endurance. It also eases the nausea, dizziness, and headaches associated with altitude sickness and relieves the symptoms of various stomach ailments. From pre-Columbian times coca has been an integral part of Andean cultures, and the commerce of coca leaves is still a legal and accepted practice in Peru and Bolivia.

Celebral Cortex And Vertigo

Exercise Illustration For Vertigo

A 43-year-old female experienced dizziness, loss of balance, some nystagmus, and ringing in the ear. A neurological exam suggested damage to a cranial nerve, perhaps associated with a small peripheral tumor. On the illustration in Question 25, which is the affected cranial nerve 38. A 70-year-old male was brought to the emergency room after experiencing headaches, nausea, and dizziness. An MRI revealed the presence of a brain tumor, which had produced a noncommunicating hydrocephalus. Which of the following is the most likely location of the tumor

Parameters Of Linkage Disequilibrium

In the previous section we introduced the squared-correlation parameter r2 as a measure of linkage disequilibrium between a pair of SNPs. Before going into the issue of estimating this parameter from genotypic information, we would like to introduce another measure of linkage disequilibrium the coefficient of association, which is denoted by D'. This measure is very popular among population geneticists. It intends at describing the relative level of linkage disequilibrium in the current population, in comparison to its level at the formation of the population. The parameter has the form of a ratio between two correlation coefficients. The numerator is the correlation coefficient computed from the given 2 x 2 table of haplotype frequencies in the population. The denominator is the correlation computed from another 2 x 2 table. The marginal frequencies of this new table are identical to those of the original table. However, one of the entries in the new table is set to be equal to zero....

The Intracanalicular Acoustic Neuroma

During the past 10 years, the long-term safety and efficacy of stereotactic radiosurgery have established this technique as an important noninvasive first-line alternative to microsurgery. The absence of procedure-related mortality and morbidity and superior tumor control, hearing, and facial preservation rates, favor radiosurgery as the first management choice for patients with intracanalicular acoustic neuromas. The Intracanalicular Acoustic Neuroma The increase in diagnosis of tumors at an early growth stage has led to controversy over management strategies. In 1994, the National Institutes of Health Consensus Development Conference determined that the treatment of patients with acoustic neuroma should be provided by an experienced multidiscipli-nary team and individualized with regard to tumor and patient characteristics.1 The individualized approach is applicable, in particular, to the management of a patient with an intracanalicular tumor. The therapeutic options available in...

Benign Paroxysmal Positional Vertigo

Benign Paroxysmal Positional Vertigo

By far the largest number of patients with true vertigo suffer from benign paroxysmal positional vertigo (BPPV). It was first described many years ago by Dix and Hallpike, but Dr. John Epley has re-investigated it more recently. He has developed a reliable curative procedure that can be done in the office. It has been found, with proven anatomic evidence, that the vertigo of these patients is due to otolithic debris (now termed canaliths) in the long limb of the posterior semicircular canal. These are displaced otoliths that are normally present over the stereocilia of the position-sensing hair cells in the utricle. Head trauma, or other less clear causes, put them in the wrong place. They create a physical drag on fluid motion in this semicircular canal, and the result is the classic symptom-complex seen in this disorder. A typical patient complains of vertigo lasting a few seconds to a halfminute when the head position changes with respect to gravity. This usually occurs when lying...

Treatment of vertigo

While nystagmus is present, patients should attempt to focus the eyes and should move and hold them in the direction that provokes the most dizziness. When nystagmus has diminished to the point that the patient can clearly focus on a target in all directions, eye-head coordination exercises should be started. A useful exercise is to stare at a target while oscillating the head from side to side and up and down. Treatment of Vertigo Benign positional vertigo Good for nausea, vertigo, more sedation, extrapyramidal effects

Circumscribed Labyrinthitis

Circumscribed labyrinthitis may be seen in patients with expanding middle ear and mastoid lesions. It is produced by localized erosion of bone into the labyrinth, without invasion of the endolymphatic portion. The usual cause is a cholesteatoma eating away at the lateral semicircular canal in the mastoid antrum, but any other expanding tumor, such as glo-mus jugulare, can be a cause. The symptom is mild vertigo, which may be aggravated by pushing on the ear or getting water in it. Positional vertigo may also be present. Complaints of hearing loss or drainage, referable to the middle ear lesion, are often present. Ear examination will uncover a middle ear abnormality. If the primary physician encounters true vertigo with evidence of middle ear disease, the ENT physician should be called immediately. A positive fistula test (see Spontaneous Perilymph Fistula in Chapter 5) is often present. There may be further erosion of the cholesteatoma or tumor into the membranous portion of the...

Orthostatic Lightheadedness

If the malaise and lightheadedness occur only within 10 minutes of the patients rising to the full standing position, then presyncope syncope from orthostatic hypotension is a probable diagnosis. There is no clear-cut vertigo, but there is often pallor, sweatiness, and a look of alarm. The patient may reach out in an effort to stabilize an upright position. Similar symptoms, even when the patient is supine, occurring in association with palpitations suggest cardiogenic hypotension from arrhythmia. However, palpitation is not always a prominent symptom.

Central Vestibular Vertigo

This type of vertigo is caused by a lesion of the vestibular nuclei, vestibulocerebellum, thalamus, or vestibular cortex, or their interconnecting fibers. Depending on the etiology (e.g., hemorrhage, ischemia, tumor, malformation, infection, multiple sclerosis, vestibular epilepsy, basilar migraine), vertigo may be transient or persistent, acute, episodic, or slowly progressive. It may be associated with other neurological deficits depending on the location and extent of the responsible lesion.

Eva Disorientation And Height Vertigo

Some EVA astronauts have described a 0-G form of height vertigo, apparently triggered by a VRI. Early reports came from Shuttle astronauts working in the open payload bay while it faced earthward. If the astronaut happened to float into an inverted orientation, looked toward their feet and saw the Earth moving by rapidly by several hundred kilometers away, their mental allocentric reference frame apparently jumped from the payload bay to the surface of the Earth below. Perceived orientation suddenly changed from floating inverted in the payload bay with the globe of the Earth above to hanging from a handrail with the surface of the Earth far below (Fig. 13-3). Figure 13-3. Floating inverted in Shuttle payload bay can cause EVA Height Vertigo (NASA photo) Height vertigo reports have also come from astronauts egressing from an ISS airlock through an Earthward facing hatch, or while standing in foot restraints on the end of the Shuttle remote manipulator arm, or while hanging on the end...

Uses in Motion Sickness

Scopolamine is useful for prevention of motion sickness when the motion is very stressful and of short duration. A transdermal preparation (Transderm-Scop) with a 72-hour duration of action has been marketed for this purpose. Blockade of cholinergic sites in the vestibular nuclei and reticular formation may account for the effectiveness of this agent. When the motion is less stressful and lasts longer, the antihistamines (H1-antagonists) are probably preferable to the antimus- carinic drugs, especially for the prophylactic treatment of motion sickness.

Linkage Disequilibrium Mapping

The genetic variants that one might be interested in mapping arise through, for example, novel mutations or immigration of carriers of mutant alleles into a population. When a mutation initially arises, it has a particular chromosomal location and specific neighbouring marker alleles. At this incipient point in time, the mutation is completely associated with the adjacent alleles it is only observed when the marker alleles are also present.51 Marker alleles that were in the neighbourhood of the disease gene when its mutation was introduced into the population will generally remain nearby over numerous generations (that is, in disequilibrium). One can estimate whether a particular marker locus appears to be in disequilibrium with a disease locus. In particular, if specific marker allele frequencies are higher among diseased versus normal chromosomes (for example, in unrelated unaffected subjects), this suggests linkage between that locus and a disease locus. The extent of this...

Disequilibrium of Aging

Disequilibrium of aging is a condition manifesting as ill-defined dizziness and gait unsteadiness. Loss of hearing and balance occur normally with age. Patients over the age of 70 may have a 20 to 40 percent loss of vestibular hair cells. In addition, elderly patients often experience a decrease in visual as well as proprioceptive input, a decline in central integration and processing, as well as a decrease in motor responses. Approximately 50 percent of individuals over the age of 70 experience imbalance of those, more than half report falls.10 The disequilibrium of aging may be precipitated or exacerbated by diminished ambient light (with worsening of symptoms at night), unfamiliar surroundings, and the use of benzodiazepines and drugs with anticholinergic effects such as tricyclic antidepressants and neuroleptic agents. The concomitant presence of near syncope or risk factors for near syncope may complicate the diagnosis.

Posttraumatic Vertigo

Closed head injuries account for a significant percentage of patients with vertigo. Vertigo or gait unsteadiness is a common complaint following a head injury. Acute posttraumatic vertigo is caused by a direct injury to the labyrinthine membranes. Its onset is immediate following the head injury, and it produces constant vertigo, nausea, and vomiting. Such patients may have sustained a concomitant fracture of the temporal bone. Vertigo immediately associated with a closed head injury warrants computed tomography (CT) or magnetic resonance imaging (MRI) to rule out an extradural or intradural hematoma. Vertigo due to direct labyrinthine trauma tends to resolve within several weeks. Closed head trauma can also displace otoconia from the utricular maculae, precipitating an attack of BPPV. Some patients with a history of a closed head injury develop a postconcussive syndrome. Although true vertigo is uncommon with this disorder, gait unsteadiness or a vague sense of dizziness are quite...

Deafness Tinnitus And Vertigo

- suppurative labyrinthitis* Trauma - petrous temporal fracture - acoustic neuroma Causes of Vertigo Causes of Vertigo i Infection - suppurative labyrinthitis viral Benign positional vertigo - transient attacks of vertigo, associated with a change in head position. Self-limiting Meni re's disease - episodic attacks of vertigo occurring in middle age, later accompanied by unilateral deafness Drugs - streptomycin, quinine, salicylates

Motion Sickness

Motion sickness was discussed earlier, but will be briefly presented here as well. Cowings and her colleagues, starting in the 1970s, conducted the early work in this area. They used physiological feedback of SCA, finger temperature, and heart rate along with au-togenic training to train individuals to increase their threshold for motion sickness. She published many controlled outcome studies and was finally given permission to train some astronauts. The individuals she trained were capable of preventing space motion sickness during their space flights without medication. She successfully extended this work to high-performance jet pilots.


The abrupt onset of vertigo after direct ear trauma such as a foreign body penetration into the ear canal should immediately prompt the diagnosis of perilymph fistula. Unfortunately such instances are rare, and more commonly, consideration of the diagnosis of perilymphatic fistula in patients with vertigo symptoms is more nonspecific. Attention to the nature of the vestibular symptoms along with onset, duration, frequency, and associated symptoms is helpful in establishing the differential diagnosis. Vertigo caused by a traumatic perilymph fistula occurs at the time of the injury and is abrupt and violent. Vertigo can last from minutes to hours and is often accompanied by nausea and vomiting. If the fistula closes, the usual recovery from the vestibular insult occurs over the next 6 to 8 weeks. Persistent vestibular symptoms after this time should alert the clinician to the possibility of a persistent or intermittent fistula. In most cases, the recurrent vertigo will not be as severe...

Antivertigo Drugs

An antivertigo drug is used to treat vertigo, which is usually accompanied by light-headedness, dizziness, and weakness. The individual often has difficulty walking. Some of the causes of vertigo include high alcohol consumption during a short time, certain drugs, inner ear disease, and postural hypotension. Motion sickness (seasickness, carsickness) has similar symptoms but is caused by repetitive motion (eg, riding in an airplane, boat, or car). Both vertigo and motion sickness may result in nausea and vomiting. It is important to note that antivertigo drugs are essentially antiemetics because many of these preparations, whether used for motion sickness or vertigo, also have direct or indirect antiemetic properties. They prevent the nausea and vomiting that occur because of stimulation of the vestibular apparatus in the ear. Stimulation of this apparatus results in vertigo, which is often followed by nausea and vomiting.

Acoustic Neuroma

An acoustic neuroma (also called a schwannoma or neurilemoma) is a tumor that arises from the neurilemma (sheath) of the eighth cranial nerve. As the tumor enlarges, it presses on surrounding nerves and interferes with blood supply. This leads to tinnitus, dizziness, and progressive hearing loss. Other symptoms develop as the tumor presses on the brainstem and other cranial nerves. Usually it is necessary to remove the tumor surgically. acoustic neuroma and characterized by hearing loss, vertigo, and tinnitus vertigo in the vestibular apparatus loosely used to mean dizziness or light-


Labyrinthitis is an infection of the labyrinth that produces peripheral vertigo associated with hearing loss. The precise etiology is often unknown. The infection may be viral, in which case the clinical course is similar to that of vestibular neuronitis. Cases have reportedly been associated with measles and mumps. Bacteria may also cause labyrinthitis. Although unusual, an infection within the labyrinth can develop from otitis media, in which bacteria and toxins diffuse across the membrane of the round window. A cholesteatoma can erode into the inner ear, creating a portal of entry for bacteria. Other possible antecedents for bacterial labyrinthitis include otitis media with fistula, meningitis, mastoiditis, and dermoid tumor. The hallmarks of this disease include sudden onset of vertigo with associated hearing loss and middle ear findings. Serous labyrinthitis may occasionally produce vertigo.


An important fact is that vertigo is the usual, but not the only, symptom pointing to the vestibular system. Disequilibrium (unsteadiness or loss of balance), without vertigo, can also be a sign of more chronic, insidious problems. In young and middle-aged patients with this symptom, certain specific diseases of the vestibular system should be ruled out. An acoustic Nonvestibular Dizziness 113 In very elderly people, dysequilibrium is more likely to indicate nonspecific multisystem deficiency, including poor circulation, poor vision, and generalized neurologic deterioration. An important clinical point should be made here. A common treatment error often occurs with this category of patients many physicians prescribe meclizine or a similar drug. This antihistamine will not help a degenerating vestibule, but will cause drowsiness Be advised that meclizine is intended for nausea and true vertigo, not imbalance.

Causes of Vertigo

Causes Benign Vertigo

The common causes of an acute attack of vertigo are benign positional vertigo, Meniere disease, and vestibular neuronitis. It may also follow head injury. Benign positional vertigo is the most frequent. It is characterized by brief (a minute or less) attacks of vertigo and nystagmus that occur with certain critical positions of the head, such as lying down or turning over in bed or tilting the head backward. Symptoms may recur periodically for several days or months. Hearing is unaffected. Diagnosis is confirmed by moving the patient from the sitting position to recumbency with the head tilted 30 over the end of the table and 30 to one side (Fig. 15-1A and B). This maneuver produces a brief attack of vertigo and nystagmus return to the sitting position changes the direction of the vertigo and nystagmus. After three or more trials, the attacks can no longer be elicited. As to pathogenesis, it is generally believed that otolithic debris comes loose from the utricular macula and, with...


The three most common causes for vertigo, unsteadiness, and disequilibrium are vestibular end organ damage and an overlong prosthesis. In years past, when the oval window was not closed with a seal, perilymphatic fistulas occurred regularly. They are fortunately now rare. Vestibular symptoms occur in the immediate postoperative period in up to 96 of cases. These symptoms seem to be less when the vestibule is manipulated to a lesser degree. Most persist for only 24 to 48 hours, but 5 may last for up to a week. Patients with evidence of balance problems in the first week should be started on labyrinthine compensatory exercises. Those who do not respond after 2 to 3 weeks should be suspected of an overlong prosthesis. Computed tomography (CT) scanning may assist in the decision to revise the case.


The primary systemic conditions causing lightheadedness affecting the heart and cere-brovascular circulation are related to anxiety or other psychiatric disorders. Sometimes, reproduction of a patient's symptoms during hyperventilation is indicative of anxiety-related dizziness these patients will often admit to generalized anxiety or even panic attack. When accompanied by horizontal nystagmus, however, the presence of cerebellopontine angle tumor must also be considered (19). A positive hyperventilation test, along with a history of cardiac arrhythmias, orthostasis, and carotid bruit, are all common manifestations of altered cerebral flow due to cardiac disease, cerebrovascular compromise, or vasoconstriction. Most commonly, extensive small vessel cerebrovascular disease is found on imaging in elderly patients with additional risk factors such as hypertension, diabetes, and hypercholesterolemia. Occasionally, dysautonomia associated with diabetes or hypoadren-alism can be identified....

Vestibular Vertigo

Acute loss of vestibular function is also called vestibular neuritis, acute vestibular neuropathy, or an acute vestibular crisis. It can be produced by a variety of pathogenetic mechanisms, the most common of which is a viral infection. The patient suddenly experiences acute rotatory vertigo with nausea, vomiting, and falling to the side of the diseased vestibular organ. Every movement of the head makes the vertigo worse therefore the patient, noting this, lies perfectly still. Examination reveals horizontally beating, spontaneous nystagmus in the direction opposite the side of the lesion, with a rotatory component. The nystagmus is more intense when the patient lies on the affected side it can be diminished by visual fixation. The affected vestibular organ is less responsive than normal to caloric stimulation. Vertigo usually resolves fully within a few days, rarely within a few hours. Often a so-called trigger labyrinth remains as a residual phenomenon, i. e., vertigo on...

Physiologic Vertigo

Physiologic vertigo is vertigo not caused by disease of the cochleovestibular system. It results from a mismatch between visual, proprioceptive, and vestibular input. This may be the pathogenesis of motion sickness as well as the transient vertigo associated with watching a film that captures the visual sensation of motion without the corresponding vestibular or proprioceptive input (visual vertigo). Visual vertigo is triggered by complex visual environments such as shopping malls and by viewing complex floor or wallpaper patterns.

Kidney Qi Vacuity Shen QiXu

General sensitivity to cold, weakness, lethargy, very susceptible to illnesses sensation of cold and weakness in lower back as well as in knees, coupled with lower back and knee pain. Gloomy mood, depression, withdrawal, fearfulness, frequent urination with clear urine, nycturia (excessive urination at night), incontinence, loss of libido, impotence, frigidity, amenorrhea (lack of menstruation), fertility disorders, hearing loss, dizziness, tinnitus, morning diarrhea, lack of appetite, soft stools.

Main Symptom Hypertension High Blood Pressure

Treatment often in connection with headache or dizziness. Caused by ascending yang, often rooted in liveryin vacuity or kidney yin vacuity. Limited treatment possibilities if hypertension has not manifested for more than one or two years. Recommended treatment Combination of acupuncture, herbs, and nutritional therapy, combined with conventional allopathic medicine. Important Weight reduction

Dangerous Supplements

Athletes at all levels should have their supplement use carefully monitored. Coaches, parents, or others working with athletes should ask what they take and in what dosage and frequency. Labels should be examined, and all information should be documented in the medical record. It is best if athletes try only one product at a time, and supplement use should be discontinued if any unusual dizziness, stomach upset, or headaches occur. All coaches should be familiar with the available supplements and their dangers. see also Dietary Supplements Sports Nutrition.

Types of Hypertension

Pregnancy-induced hypertension (PIH) may appear in otherwise healthy women after the twentieth week of pregnancy. It is more likely to occur in women who are overweight or obese. PIH may be mild or severe, and it is accompanied by water retention and protein in the urine. About 5 percent of PIH cases progress to preeclampsia. Preeclampsia is characterized by dizziness, headache, visual disturbance, abdominal pain, facial edema, poor appetite, nausea, and vomiting. Severe preeclampsia affects the mother's blood system, kidneys, brain, and other organs. In rare cases, the woman can die. Preeclampsia is more likely to occur during first pregnancies, multiple fetuses, in women with existing hypertension, and in women younger than twenty-five years old or over thirty-five years old. If convulsions occur with PIH, it is called eclampsia. PIH disappears within a few weeks after birth.

Other diseases of the intestinal epithelium

They are small for gestational age and have an abnormal phenotype.11 All have facial dysmor-phism with prominent forehead, broad nose and hypertelorism. They have a distinct abnormality of hair, tricorrhexis nodosa, in which the hair is woolly, difficult to manage, easily pulled out and poorly pigmented, even in children of Middle-Eastern origin. Among the congenital forms of hair dysplasia, tricorrhexis nodosa is very common, and can be present in several pathological conditions.61-64 In addition, the previously reported patients had defective antibody responses despite normal serum immunoglobulin levels, and defective antigen-specific skin tests despite positive proliferative responses in vitro.12 Small-bowel biopsy specimens of the patients with diarrhea syndrome show moderate or severe villus atrophy with inconstant mononuclear cell infiltration of the lamina propria, and absence of epithelial abnormalities. Histologically, there are no specific abnormalities. The prognosis of...

Zollinger Ellison and pseudoZollinger Ellison syndromes

'PZES' is usually used for two distinct entities antral G-cell hyperplasia, described as an increased number of G cells, and antral G-cell hyperfunction, in which hypergastrinemia occurs in the absence of detectable G-cell hyperplasia.38 The clinical manifestation of PZES varies from vague features, such as non-specific abdominal pain, vertigo, anemia and occult bleeding, to severe gastrointestinal bleeding. The differentiation between ZES and PZES is based on the response to provocative tests. PZES is characterized by exaggerated serum gastrin release in response to a feeding test, and unchanged or even depressed serum gastrin values after injection of secretin.

Functional bowel disorders presenting with abdominal pain

Although the terminology seems confusing, it should be noted that the term 'functional abdominal pain' has been considered by the Rome II committee members as one of the categories of abdominal pain, being an entity by itself (Table 14.1). This group comprises patients with pain that is usually located in the periumbilical region and is not consistently related to eating, defecation, menses, or exercise. Patients may have associated headache, dizziness, light-headedness, nausea and vomiting. As with other forms of pain of functional origin, the diagnosis is clinical.

Have a specific objective in mind when starting a new routine

No matter what activity you choose, always warm up and cool down. Warming up promotes blood flow and gets your muscles and joints primed to handle a fat-burning workout. The cool down gets rid of metabolic wastes, like lactic acid (the chemical that is associated with muscle soreness, keeps blood from pooling in specific areas (which could lead to dizziness or fainting), and, along with light stretching, keeps your muscles limber.

Boost Alertness Memory and Beat Stress

Army researchers looked into the effects of supplemental tyrosine, the precursor to dopamine, epinephrine, and norepinephrine (the major players in the brain's response to stress). When given tyrosine supplements, soldiers exposed to high altitudes or prolonged cold did not suffer the loss of memory, lightheadedness, headache, nausea, and general malaise such stresses normally bring on.

Cervical Spondylopathy

Clinically, symptoms of cervical spondylopathy are miscellaneous however, those such as pain or numbing pain in the neck, shoulders (including their periphery, upper part of the back and chest and upper extremities due to irritation or compression of cervical nerve roots are common.Cervical overstrain or exopathic cold may serve as factors inducing this disease or worsening its symptoms. If the spinal cord is irritated or compressed, symptoms of numbness and weakness of the lower extremities, and staggering gait may appear while if vertebral artery is irritated or compressed, vertigo and dizziness may appear.

Clinical Manifestations

Chronic hepatitis can be divided into chronic delaying hepatitis and chronic motative hepatitis. The symptoms of the former include a poor appetite, tiredness, weakness of the lower limbs, enlargement of the liver, which is painful upon being pressed. The symptoms of the latter include a pain in the liver area, dizziness, sleeplessness, long-term fever, loss of weight, abdominal swelling and pain of the joints. Both types are found abnormal in the liver functioning test at different

Administration of HO and metabolite sampling

For both safety and practical purposes, body-water 2H-enrichment levels in humans is limited to 0.3-0.5 mol . For attainment of 0.5 mol body-water enrichment in a 75 kg male, a loading dose of 253 grams of pure 2H2O is required (assuming body water content is 60 of bodyweight. For females, body water content is assumed to be 50 of bodyweight). The development of transient vertigo - sometimes accompanied by mild nausea - is a well-documented effect of drinking a bolus of highly enriched deuterated water. To avoid this, the loading dose is divided into two or three portions, which are taken over a 1-2 h period. The deuterated water can be made more palatable by dilution with around two volumes of bottled spring water to give a 33 -enriched solution. The additional water does not significantly dilute the body water enrichment. Body water enrichment is maintained over the duration of the study by providing drinking water with the same 2H-enrichment as the target enrichment level. Steady...

Looking for Hypoglycemia

Your signal to check may include shakiness, nervousness, sweating, chills and clamminess, rapid heartbeat, trouble concentrating, headache, dizziness, light-headedness, moodiness, clumsiness, tingling in your face or lips, extreme hunger, or irritability. These symptoms can happen at any time. You could even wake up in the middle of the night with a nightmare because of hypoglycemia.

Treatment for erectile dysfunction

Food and Drug Administration began to receive reports of sudden loss of hearing in men taking the drugs described above. Some of the men also reported dizziness and ringing in the ear. The hearing loss was temporary in one third of cases and too recent in the others. It begins within hours to a day or two of starting these drugs. It involves only one ear. There have been only 29 cases among the millions who have taken the drugs beginning in 1996. If you experience hearing loss, take no more of the drug and report it to your doctor. Since the side effect is so rare, it should not prevent you from using the drugs, but you should be aware of it.

Surgery for weight loss

Formerly, the best surgical treatment for obesity was the vertical banded gas-troplasty, where the upper stomach is stapled to create a small, thumb-sized pouch above, a narrow opening, and a larger pouch below. Because the upper pouch is small, you have a feeling of early fullness, and you tend to eat less. The upper pouch is connected to the small intestine so that the lower stomach is bypassed. Patients are forced to eat very small portions and can't eat sugar and other carbohydrates, which cause dizziness and other symptoms. Most of the weight is lost in the first year.

What is the therapy for peripheral neuropathy

Gabapentin is a g-aminobutyric acid analogue and is used for treating focal convulsions. Administered at a dose of 900-3600 mg day, it is quite effective in ameliorating neuropathic pain. It has the advantage of lacking side effects and interactions with other medicines and thus it has been extensively used in the symptomatic treatment of painful diabetic neuropathy. Furthermore, it is the only medicine of its class that has been officially approved for administration in this condition. In two recent randomized studies, gabapentin was compared to amitripty-line. The first study showed equal effectiveness in ameliorating pain, whereas the second displayed the superiority of gabapentin. Most frequent side effects are sleepiness and dizziness, with a feeling of tiredness less frequently reported. These side effects usually occur after initiation of therapy, but subside with its continuation.

How do you treat the patient

A 34 year old patient with Type 1 DM for 30 years reports dizziness and fainting tendency when standing for a few minutes. These symptoms are more intense when standing up from supine or sitting position, after eating and after injecting his insulin. He is suffering from diabetic nephropathy (creatinine 2.5 mg dl 221 imol L ) and bilateral proliferative retinopathy treated with photocoagulation. Apart from insulin, he also receives ACE inhibitors for his nephropathy and coexistent hypertension. What is the diagnosis Most likely this patient is suffering from orthostatic hypotension. Orthostatic hypotension is defined as the fall in systolic blood pressure by more than 30mmHg (or according to some authors by 20mmHg together with symptoms) or the fall of diastolic blood pressure by more than 10mmHg, when assuming an erect from supine position. It is characterized by dizziness, weakness, visual disturbances, fainting spells or even loss of consciousness at erection from supine or sitting...

Can we cure erectile dysfunction

Another medicine that is also available for this problem is apomor-phine. Apomorphine stimulates the paraventricular nucleus in the brain. When used sublingually (2 and 3 mg) it acts after 20 minutes. The results in diabetic individuals are not encouraging. The main undesirable effects are nausea, headaches and dizziness.

Symptoms in Elderly People with Type Diabetes

Logical' in nature and included unsteadiness, lightheadedness and poor concentration (Table 10.5). Trembling (71.2 ) and sweating (75 ) also featured prominently, contrasting with a Canadian study in which it was claimed that the autonomic symptoms of hypoglycaemia in the elderly were attenuated (Meneilly et al 1994a). However, the latter study did not use an age-specific symptom questionnaire, and differences in symptom questionnaires and in scoring methods of inducing hypoglycaemia may account for the differences in symptom profiles that have been described.

Genetic Variations and Diabetes

There are two general methods used to locate diabetes genes, that is, linkage study and association study. A linkage study examines the genome regions shared by affected relatives, based on the coseg-regation of genes found together in close proximity on a chromosome. An association study examines the coexistence of genetic markers with the disease. There are two types of association study, that is, the population-based study using a case-control format and the family-based study using the transmission disequilibrium test (TDT). Compared with the family-based study, the population-based study has relatively higher statistical power, that is, less demanding on the sample size. However, the population-based study can suffer from bias from population stratification. Population stratification occurs when there are multiple subgroups with different allele frequencies within a population. The different underlying allele frequencies in sampled subgroups might be independent of the disease...

Presentation of CHD in Diabetes

Diabetic patients may experience symptoms caused by CHD in the same way as non-diabetic patients. Other symptoms attributable to obstructive CHD include breathlessness, manifesting as 'angina-equivalent', and ischaemia-related left ventricular dysfunction. Palpitations, presyncope and syncope may arise because of ischaemia-related arrhythmia, such as atrial fibrillation flutter, and ventricular arrhythmia, including ectopy and tachycardia. A characteristic feature of diabetes is the absence or muted intensity of angina. This 'silent ischaemia' is partly related to diabetic autonomic neuropathy (Findlay, 2003). The prognosis of patients with 'silent ischaemia', as evidenced by ischaemic changes on an electrocardiogram (ECG) on exercise testing without symptoms and good prognostic features, is similar to those with symptomatic angina (Lotan etal., 1994 Marwick, 1995).

Clinical Implications

Orthostatic hypotension (defined as a fall in systolic or diastolic blood pressure in excess of 20 mmHg or 10 mmHg, respectively with symptoms 58 ) is a consequence of cardiovascular denervation and might reflect the consequences of a fixed resting heart rate and impaired visceral and lower limb vascular tone. The normal increase of plasma norepinephrine on standing is often attenuated in CAN (59). Symptoms can vary from intermittent dizziness, to visual impairment, and syncope. The diurnal variation of blood pressure is decreased in CAN subjects, and may contribute to nocturnal supine hypertension and nephropathy (60).

Clinical Manifestations Of Oh

OH is manifested as a constellation of symptoms that develop on standing and dissipates on lying back down. Lightheadedness is common, but other symptoms are also very common. These include a sense of weakness, especially of the legs, and difficulty thinking clearly. Pain in the neck and trapezii (coat hanger headache) occurs in about 20 of patients. It was evaluated in a prospective study, 90 patients with symptomatic OH, 60 patients with symptoms but without laboratory confirmation of OH, and 5 patients with asymptomatic OH. Although lightheadedness is common about 50 of patients more than the age of 60 have problems of cognitive impairment on standing that clears on sitting or lying down (25). Cognitive problems are typically more obvious to the companion than the patient, although not infrequently the patient will use terms like I feel goofy, at least in Minnesota. Some patients complain of a retrocollic heaviness or headache on continued standing (26). The patient may feel faint...

Treating Hypoglycemia

Having help available when needed is important. The person's family members, coworkers, or other trusted people should learn to recognize the symptoms of hypoglycemia and know how to treat it if necessary. Symptoms of hypoglycemia are dizziness, sweating, feeling shaky or faint, clamminess, rapid heartbeat, clumsiness, moodiness, and extreme hunger. However, each person should know his or her own particular symptoms since everyone reacts differently.

Symptoms in Children and Older People

Dizziness frequently reported symptoms of behavioural disturbance such as irritability, argumentativeness and aggression. This latter group of symptoms is not prominent in adults, although the Edinburgh Hypoglycaemia Scale includes 'odd behaviour' as an adult neuroglycopenic symptom. Others had previously noted the prominence of symptoms such as irritability, aggression and disobedience in the parents' reports of their children's symptoms of hypoglycaemia (Macfarlane and Smith, 1988 Macfarlane et al., 1989). Parents tend to under-report the subjective symptoms of hypoglycaemia, such as weakness and dizziness, but generally there is good agreement between parents and their children about the most prominent symptoms of childhood hypoglycaemia (McCrimmon et al., 1995 Ross et al., 1998).

Obesity and cardiovascular disease

The structural and functional changes are also seen in the right side of the heart in obesity. Right ventricular dysfunction could be secondary to left ventricular dysfunction or due to obstructive sleep apnoea and or obesity hyperventilation syndrome which occurs in 5 per cent of morbidly obese individuals (Alpert and Hashini, 1993).

Preventing or slowing renal impairment

Tight control of hypertension slows deterioration of renal function in nephropaths. This means treating people whose blood pressure would not normally fall into the treatment range for non-diabetic people. In patients with known diabetic kidney disease the aim is to keep the blood pressure below 125 75 but be careful to avoid dizziness and falls in patients with severe postural hypotension due to autonomic neuropathy.

Examination Of Candidate Genes For Diabetic Nephropathy

Besides linkage studies for chromosomal regions harboring susceptibility genes for DN and subsequent positional cloning of the putative genes in those regions, an alternative strategy currently employed by many investigators is the candidate gene approach (7,37). Unlike genome scans that do not require prior knowledge of the biology of the susceptibility gene, this approach is hypothesis-driven because it focuses on proteins suspected of involvement in the pathogenesis of DN. A gene encoding for one of these proteins is screened for the presence of DNA polymorphisms (single-nucleotide polymorphisms SNPs , insertion deletions, or microsatellite markers). Then the distributions of alleles and genotypes of these polymorphisms are examined in unrelated diabetic patients with nephropathy (cases) and unrelated diabetic patients who have remained free of DN despite a long duration of diabetes (controls) to determine whether there are differences. If the groups of cases and controls are...

Considerations Regarding Examination of Other Candidate Genes

If an association is found in case-control studies, and is supported by family studies, it may be inferred that the DNA polymorphism is a marker of genetic susceptibility to DN. However, the biological interpretation of the association is not always clear. It may be owing to the polymorphism itself, including a disease-causing allele that directly affects the expression or function of a gene or gene product (e.g., by an amino acid change, frameshift mutation, or premature termination), or the association may result from linkage disequilibrium between the marker polymorphism and a causative polymorphism. This phenomenon is owing to the fact that particular alleles of polymorphisms lying in close genetic proximity to each other have a tendency to segregate together over successive generations (70). Therefore, whereas association between a polymorphism and DN may be demonstrated, confirmation that the polymorphism is actually the cause of genetic susceptibility can only be obtained from...

Positional Cloning of Type Diabetes Genes

These genome scans have mapped loci within large chromosomal regions containing 10-20 million nucleotides. Now the challenge is to identify the diabetes-related genes within this interval. The classical approach, that consisted in building up a physical map of the region through contiguous artificial chromosomes spanning the entire region of linkage, followed by the cloning of the gene, is limited by the size of the regions of linkage. An integrated genomic approach might be needed. It would combine linkage disequilibrium

The Search For Novel Nonmhc Susceptibility Genes

Recent genomewide searches for T1DM susceptibility provided preliminary evidence for the existence of at least 18 loci associated with T1DM (164). Because of the large number of markers tested, many of these putative regions suggestive of T1DM susceptibility linkage may have occurred by chance. Saturating the putative locus with many more informative markers is a must to demonstrate or rule out the existence of significant linkage. Further complicating the issue of suggestive linkage from genomewide scans is the broad range of selection criteria used for inclusion of families in the various datasets. Variations in the age of onset of T1DM can make the detection of linkage difficult. Confounding matters even more is the interaction of the various disease susceptibility loci that is the hallmark of polygenic diseases like T1DM, in that this interaction (additive, multiplicative, or epistatic) adds an additional level of difficulty in determining the significance of a logarithm of odds...

Cardiovascular Autonomic Neuropathy

Postural hypotension produces weakness, dizziness, visual impairment, and syncope that are at times difficult to distinguish from hypoglycemia or vertigo. Orthostasis results from a combination of both central and peripheral cardiovascular sympathetic denervation and is defined as a fall in systolic blood pressure in excess of 30 mm Hg. It results in part from a failure of vasoconstriction in both splanchnic and peripheral vascular beds. There is a loss of diurnal variation of blood pressure in patients with DAN, with nocturnal supine hypertension, which may also be evident to a lesser degree in healthy diabetic patients (121). Patients with a profound disability resulting from postural hypotension are, fortunately, rare. There can be a great day-to-day variability of orthostatic symptoms, which may be aggravated by insulin therapy (122) and food (123). The mechanism of postprandial hypotension in DAN is unclear, but vasodilatory gut peptides have been implicated. A hematocrit should...

Introduction And Prevalence

This review summarizes the current therapeutic approach to diabetic ketoacidosis and hyperosmolar coma. The focus is on emergency treatment and intensive care management, particularly with regard to volume substitution, insulin therapy and potassium replacement. The basic concepts of low and very low insulin therapy are presented, with special emphasis on the pathogenesis and avoidance of the disequilibrium syndrome. Furthermore, the indications for bicarbonate therapy as well as phosphate and magnesium replacement in diabetic ketoacidosis are discussed. Until the introduction of substitution therapy with insulin in the 1920s, the diabetic coma was the inevitable cause of death for all patients with type 1 diabetes mellitus and for many patients with type 2 diabetes. During the following decades, high-dose insulin therapy was wide-spread. Today, therapy of diabetic ketoacidosis is differentiated with the combination of low dose of insulin and avoidance of disequilibrium syndrome by...

Complications And Avoidable Mistakes In Therapy

In the treatment of diabetic coma several potentially avoidable complications can appear (Table 7). In particular, syndrome disequilibrium associated with cerebral edema is caused by an overly rapid fall of osmolality, especially by hypotonic solutions and inadequate bicarbonate therapy. Hypernatremia and hyperchloremia can be induced by excessive infusion of sodium chloride, especially with decreased renal function and infusion of sodium bicarbonate. If there is a lack of monitoring of central venous pressure, volume therapy can lead to pulmonary edema. Over dosage of bicarbonate can induce paradoxical acidosis of the central nervous system. Hypokalemia appears frequently after rapid application of a high insulin dose and inadequate potassium substitution. Phosphate depletion in disturbed renal function and lack of balance can lead to individual problems and hypocalcemia can be the consequence of a high phosphate substitution. High insulin replacement increases the risk of...

Special Features Of Hyperosmolar Nonketotic Coma

Comparably to diabetic ketoacidosis the primary aim of therapy should be the slowly lowering of blood glucose by about 50 mg dL per hour and the avoidance of osmotic disequilibrium with concomitant brain edema (11). If plasma osmolality can be measured, the rate of lowering should not be higher then 5 mOsm L per hour. Therapeutically, volume therapy is the first step with ringer-solution or isotonic saline solution in the amount of 1 L hr. The following volume therapy should be adjusted to central venous pressure. Hypotonic fluid substitution with 0.45 isotonic saline solution or half-half-solution (saline solution vs. glucose 5 ) should be considered. An initial insulin therapy can be retarded as long as blood glucose decreases only by fluid replacement. Potassium substitution is necessary as described in ketoacidotic coma. As said before, once a blood glucose of 250 mg dL is reached, further reduction would be performed very slowly to avoid disequilibrium syndromes (8,11). Many...

Evaluating The Patient For Autonomic Symptoms And Signs

Evaluation of patients for autonomic dysfunction should start with a careful review of symptoms. Several symptoms are useful indicators of the possibility of autonomic nervous dysfunction. These symptoms include postural dizziness, lack of sweating, failure of erection or ejaculation, difficulty with emptying the urinary bladder or recurrent urinary tract infections, and dryness of the eyes, mouth or vagina. Table 2 shows the implications for sympathetic and parasympathetic dysfunction in such patients. An infrequently sought symptom in patients with diabetic autonomic neuropathy is gustatory sweating of the face, which reflects parasympathetic denervation. Postprandial hypotension is unlikely to occur except in severe autonomic neuropathies. It results from pooling of blood in the viscera and is aggravated by abrupt standing after meals. Fainting, orthostatic dizziness

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