Vitamins and Minerals

By: | Post date: May 26, 2017 | Comments: No Comments
Posted in categories: Health

In 1990, Sheldon Saul Hendler MD, PhD, a biochemist at the University of California wrote, “Although consumption of the so called well-balanced diets still thought by some to supply all the vitamins (and minerals) we need in quantities sufficient for the maintenance of good health, there are many situations that place people at and increased risk for vitamin (and mineral) insufficiency (deficiency) states. Among those at risk are alcoholics, people on low-calorie diets, pregnant women, the elderly in general, surgical patients, users of certain medications and strict vegetarians.There are essential vitamins and minerals in pharmacological doses, which are highlighted in the table, to be taken in order to prevent progression of the diseases. Multivitamins should be taken daily by everyone over 50 years old, yet they all contain much lower amounts than required to function as antioxidants and anti-homocysteine.

Supplements, theoretically should help, but must not be, considered a substitute for and adequate diet, but they offer both assurance and insurance (prevention) that the individual is getting enough to remain healthy. All deficiencies have a beginning and are silent until overt symptoms develop. This is because we cannot read or recognize intracellular events, which is where they do their thing, that is function at the biochemical level. The occurrence of symptoms is natures way of waking us up.


By: | Post date: May 22, 2017 | Comments: No Comments
Posted in categories: Health

Dizziness is a commonly encountered complaint in the emergency department (ED) and accounts for approximately 1.5% of all hospital admissions. [13] [35] [40] In one survey, 26% of all ED patients stated that they had experienced dizziness. [28] Dizziness may be the most common non-pain-related physical complaint seen in the ED. In primary care practices, it is reported that dizziness accounts for 8 million outpatient visits per year in the United States. [40] In fact, all people experience dizziness at some point during their lives. If dizziness is so frequently encountered, what precipitates a patient with dizziness to present to the ED? There are two primary reasons why people experiencing dizziness present to the ED: (1) it interferes with their normal daily activities, and (2) the patient is concerned that they might have a serious underlying disease process. [41] [51]

Dizziness is uncommon in children, but becomes more common in adults as a function of age. In fact, dizziness affects more than 50% of elderly patients and is the commonest complaint of patients over 75 years of age. [26] In the elderly, dizziness can lead to falls and significant injuries. When troubled by dizziness, older patients often refrain from physically strenuous activities, social events, and travel. Accordingly, a fear of dizziness can cause these senior citizens to withdraw socially and facilitate their functional decline. [8] [25]

For many emergency physicians, the clinical evaluation of dizziness is a difficult and perplexing task. The primary reason for this frustration is because dizziness is a nonspecific symptom that describes a subjective sensation that is virtually impossible to objectively measure. Patients use the term dizziness to describe a perception of altered variation in spatial awareness. [3] This perception ranges from a general sense of illness, to fatigue, weakness, lightheadedness, fainting, disequilibrium, or an illusion of motion (vertigo). The cause of these perceptions can range from labyrinthitis to cerebral hemorrhage to cardiac arrhythmias to orthostatic hypotension to volume depletion. It is readily apparent to the clinician that the ability to rapidly focus on one organ system dysfunction to explain or account for the patient’s presentation is not possible–especially in the aged. Multiple systems maintain the proper perception of the relationship between the person and the environment. These systems include the vestibular, visual, and proprioceptive systems. Accordingly, the differential diagnosis can be quite lengthy. Regretfully, there is no quick and simple method to identify patients, especially older patients, at risk for “serious” causes of dizziness.

The purpose of this article is to present a systematic approach to the evaluation and management of the dizzy patient from the perspective of the emergency physician, with an emphasis on a management strategy that is timely and cost effective. Subsequently, obtaining a precise and accurate history and physical examination cannot be stressed enough, because in the evaluation of this complaint, laboratory tests and imaging studies are of little, if any, diagnostic value. The first portion of the article focuses on adults, particularly the geriatric patient, and the second portion of the article concentrates on pediatric patients.


The most useful diagnostic approach is to determine whether the patient’s complaints arise from an inner ear disorder, a brain disorder (brainstem or vestibulocerebellum), both, or neither. The first three categories may be considered vestibular disorders and the last considered nonvestibular. [9]
Patient History

The evaluation of the dizzy patient begins with obtaining a meticulous and accurate history. In fact, the patient history is the most important part of the entire patient evaluation. [4] Taking the time to obtain a factual history is crucial because it often helps to distinguish between vestibular and nonvestibular etiologic factors and directs further assessment.


First and foremost, determine the patient’s definition of dizziness, because dizziness means different things to different people. [38] Also, dizziness is a colloquial term that may have many synonyms depending on the age of the patient and the geographic or ethnic background. Ask what they mean by the use of the term dizziness, without the use of leading questions or suggesting an explanation. This can best be accomplished by asking an open-ended question such as “Can you describe this dizziness?” Then one should wait for the patient’s answer–without any type of explanation. Caution should be used when interviewing patients with dizziness because they tend to be suggestible and it is very easy for leading questions to deliver a erronious or misleading history. The most useful historical information is the patient’s own description of his or her dizziness, its characterization, and the effects of position on the patient’s symptoms. [49]Subsequently, the patient who complains of vertigo should be assessed as though the complaint were dizziness. Patients should be encouraged not to use medical terminology when describing their symptoms. Obtaining such an open-ended history from older patients can take a significant amount of time and can be taxing. In this clinical setting, the examiner must recognize the general trend of the problem and determine if the dizziness is getting better, worse, or staying the same. [5]

Characteristics and Qualities of Symptoms

Vestibular disorders (inner ear and/or brain) almost always present with the patient perceiving a spinning sensation. Patients with vestibular lesions often compare the sensation to that of being drunk or having motion sickness. They also may describe feelings of imbalance, as though they are falling or tilting to one side. Many clinicians automatically associate descriptions of spinning or swimming with vertigo. It is important to delineate that the patient actually perceives a sensation of abnormal motion (rotation) of either the surroundings or of the body. This sense of rotation can be clockwise, counterclockwise, horizontal, or vertical. The patient with dizziness of functional origin is more likely to describe an internal spinning within the head, rather than the sensation of the external environment’s spinning. [16] True vertigo is defined as a clear sensation of rotation of oneself in relationship to the environment. [48] By this definition, vertigo strongly implies a neural dysfunction of the inner ear, brain stem, or the vestibulocerebellum. For the remainder of this article, vertigo is referred to as a vestibular disorder (VD).

Patients with nonvestibular disorders (NVD) usually describe dizziness with such terms as light-headed, floating, weakness, wobbly, giddy, woozy, sinkin’ spell or some other colloquial term to describe a state of decreased cerebral perfusion. This inadequate blood flow to the brain can be mediated by decreased cardiac output (e.g., valvular heart disease, cardiac arrhythmias, cardiomyopathies), volume depletion (e.g., gastrointestinal hemorrhage, anemia), orthostatic hypotension (e.g., drugs), structural blockage of arterial flow to the brain, or a metabolic cause. A vague spinning sensation without true vertigo most likely indicates a nonvestibular disorder. The sensation that one has left one’s body is characteristic of psychogenic dizziness. [46]

Aggravating/Relieving Factors

Many authorities feel that it is equally important to ask the patient about the circumstances or activities that exacerbate or alleviate the dizziness, which can give valuable clues whether the dizziness is vestibular or nonvestibular. The most notable activity that distinguishes VD from NVD is positional changes; however, dizziness related to change in position may be misleading. Certain positions of the head or body may trigger vestibular conditions such as benign positional vertigo, but nonvestibular causes of dizziness, such as orthostatic hypotension or anemia, can also be positional. The clinician must be careful to ensure that the change in position involves just the vestibular structures, as opposed to activities that diminish cerebral blood flow. [45] The tendency to list or lean to one side, an aggravation of symptoms by turning over in bed or closing one’s eyes, a sense of imbalance when making a quick turn on foot or in a car, and the reluctance to bend over suggest VD. Also, vertigo that is worsened by loud noise suggests a vestibular etiology. [43] Symptoms worsened by Valsalva’s maneuver can also be noted with a vestibular lesion. [43] Dizziness of vestibular origin occurs spontaneously and is usually exacerbated by head movements. Vestibular dizziness may be provoked when the head is moved into a certain position, such as after vertical and oblique head movements when lying down or sitting up.

Nonvestibular dizziness may be provoked by standing up after lying down for at least 2 minutes. If dizziness is induced primarily by eye movements when the patient’s head is still and if the patient does not have an eye movement disorder, the dizziness is probably not caused by a vestibular problem. In other words, vertigo is typically aggravated by head movements, whereas NVD is often aggravated by movement of visual targets. [39] Furthermore, symptoms that increase with exercise suggest NVD. Additionally, VD may become more symptomatic with exercise-associated head movement. Although stress can aggravate both vestibular and nonvestibular dizziness, dizziness that is consistently precipitated by stress suggests a nonvestibular cause. Finally, episodes of dizziness occurring in specific situations (e.g., driving on a busy freeway, during arguments, etc.) suggest a nonvestibular cause. [10]

Associated Symptoms

A multitude of symptoms may coexist with dizziness, and the coexistence of these symptoms helps to determine the cause of the dizziness and guide the clinician toward diagnostic as well as therapeutic intervention. Some of the more significant concomitant symptoms are altered mental status, headache, hearing loss, tinnitus, nausea and vomiting, visual disturbances, focal motor/sensory deficit, and ataxia.

Altered mental status in the setting of NVD may be attributed to drug toxicity, cardiac arrhythmias, metabolic disorders, severe anemia, or the many conditions that can cause hypotension. Altered mental status in the setting of VD indicates a life-threatening emergency that mandates a rapid diagnosis and treatment (i.e., cerebellar hemorrhage or infarction).

Headache associated with dizziness (regardless of whether it is VD or NVD) always raises the concern for a CNS infection (meningitis), intracranial hemorrhage, cerebral aneurysm, migraine cephalgia, and a systemic or febrile illness.

Hearing loss is frequently found in VD and is usually labyrinthine in origin. Sensorineural hearing loss occurs with disorders of the inner ear or along the nerve pathway to the brain stem. Conductive hearing loss is caused by disorders of the outer and middle ear. Central hearing loss transpires with lesions in the central auditory pathway beyond the eighth cranial nerve.

Tinnitus, or a ringing or roaring in the patient’s ear, is an important symptom. Inquire in which side or ear it is located and its character: continuous, intermittent, or pulsatile. One must establish the presence of a pulsating sound versus a continuous or intermittent tinnitus. One must also ask about a hearing loss in the same ear because tinnitus in association with a hearing loss in the same ear is suggestive of VD. Rarely, tinnitus actually can be heard by the examiner. The differential diagnosis for this objective tinnitus is a glomus tumor, lesion of the cerebellopontine angle, aneurysm of the internal carotid artery, or a high-riding jugular bulb.

Nausea and vomiting are nonspecific findings that may be found in VD as well as NVD; however, nausea and vomiting that are of sudden onset and quite debilitating tend to be VD (labyrinthine) in origin. Visual disturbances such as diplopia and loss of vision in combination with dizziness are suggestive of a VD, whereas blurring of vision correlates with NVD. Focal motor/sensory deficit in affiliation with dizziness is characteristic of focal CNS nervous system lesions; however, diffuse weakness and numbness tend to be NVD. Ataxia or disequilibrium represents a loss of vestibulospinal, proprioceptive, or cerebellar function. Common causes include ototoxicity, peripheral neuropathy, stroke, or a VD.

Timing and Duration of Symptoms

Vertigo almost always occurs in episodes, is usually sudden in onset, and decreases in magnitude as the precipitating factor fades away or as compensation occurs. Duration of episodes associated with the most common causes of vertigo are as follows: seconds–benign positional vertigo; minutes–cerebrovascular ischemia; hours–Meniere’s syndrome; days–viral labyrinthitis. All of these causes are VD. [42]

Conversely, certain types of NVD also exhibit a typical pattern of duration or occurrence. Common causes of episodic lightheadedness that typically lasts minutes include postural hypotension, vasovagal reactions, and cardiac arrhythmias. Lightheadedness can also be episodic or continuous. Chronic continuous lightheadedness is common with hyperventilation syndrome. Vertigo on first arising in the morning is called matutinal vertigo and is usually due to a peripheral vestibular disorder. [7]

Predisposing Factors

The medical history is very important when one is evaluating underlying diseases or traumatic processes that provide a foundation for the occurrence of dizziness. Many systemic disorders are associated with dizziness due either to the involvement of the CNS or to the impaired ability to assimilate the sensory input. Hypertension, diabetes mellitus, seizure disorder, and septicemia are prime examples of diseases that meet these criteria. Trauma to the labyrinth may occur directly through a temporal bone fracture, a whiplash injury, or as a result of a closed head injury. This form of dizziness may take up to a year to resolve. Furthermore, a fistula between the middle ear and inner ear may occur secondary to trauma. A history of chronic ear infections may predispose to the formation of otosclerosis or a cholesteatoma and the subsequent development of dizziness. A careful drug history is critical when assessing any patient who complains of dizziness. The number of drugs that cause orthostatic hypotension is legion. The social history also provides valuable information by identifying tobacco, alcohol, and illicit drug use patterns. The sexual history may reveal activities that predispose for contracting syphilis, AIDS, and other CNS diseases. [12]
Physical Examination

After taking such a detailed history, the clinician should be able to perform a selective or focused physical examination. The patient who is complaining of VD should have emphasis placed on the ears, eyes, and neurologic components of the physical examination. Likewise, the patient complaining of NVD should have special attention to metabolic and cardiac elements of the physical examination. Unfortunately, there will be patients who are poor historians and do not give a distinct impression of vertiginous versus nonvertiginous dizziness, but who have symptoms suggestive of both. In such patients, the physical examination will need to be as thorough and complete as the history.

Key elements of the physical examination are

VIII. A. 1.

Vital Signs (to include orthostatic vital signs):
Blood pressure: Hypertension, especially when poorly controlled, can elicit VD. Patients with uncontrolled hypertension are prone to arterial spasm, reducing blood flow to the labyrinth (vertebrobasilar insufficiency). Also, with uncontrolled hypertension an artery may rupture into the labyrinth, causing VD. Hypotension can cause NVD from inadequate cerebral perfusion.
Blood pressure in both arms: A discrepancy of greater than 20 mm Hg in both arms may detect a thoracic dissection, aortic coarctation, subclavian steal syndrome, or other vascular pathologies that may result in diminished cerebral perfusion. The subclavian steal syndrome aggravates NVD by arm movement.
Orthostatic vital signs: Orthostatic hypotension, defined as a drop in systolic blood pressure of 20 mm Hg or more within 2 minutes of assuming an upright posture, is a feature of NVD that can be attributed to drugs, volume depletion, anemia, or other mechanisms that result in diminished cardiac output or decreased cardiac return.
Heart rate: A significantly fast (>150 bpm) or slow heart rate (<40 bpm) can account for NVD.E. Respiratory rate: Hyperventilation is notorious for causing NVD and is usually psychogenic in origin. Hypoxia can also elicit NVD.
Temperature: A febrile state, whether secondary to an infection or systemic disease, has long been recognized as a cause of dizziness (NVD).
Mental Status: Altered mental status in conjunction with NVD may be attributed to metabolic abnormalities, drug toxicity, or CNS infection. Altered mental status with VD signals a life-threatening emergency that calls for a rapid diagnosis as well as treatment (i.e., cerebellar hemorrhage or infarction).
Head: Initially, the head should be evaluated for signs of trauma. The geriatric patient may be a victim of elder abuse or may have sustained a head injury secondary to a fall. Furthermore, inadequate blood flow to the brain is a significant cause of VD and NVD in the elderly. Bruits in the head region are never considered to be normal in adults. The head should be auscultated for bruits (using the bell portion of the stethoscope) over the following regions: carotid artery from the supraclavicular area to the base of the skull, over both eyes closed (bruits are transmitted through the orbital fissures), just anterior to the ears over the squamous portions of the temporal bones, and at the mastoid processes.
External auditory canal: Wax or cerumen impaction, foreign body, vesicles of herpes zoster (Ramsey Hunt syndrome).
Tympanic membrane: Fluid, retraction, infection, sclerosis, perforation, hemotympanum, CSF otorrhea, or cholesteatoma.
Mastoid: Edema, erythema, ecchymosis, or tenderness over the mastoid region. Auscultate for bruits.
Pupils: Aniscoria is indicative of a central CNS lesion. Assess CN II.
Extraocular muscles: Assess function of CN III, IV, and VI.
Spontaneous nystagmus: Patients with spontaneous nystagmus (horizontal, rotary, or both) have VD (peripheral or central). Patients with vertical nystagmus have central lesions. It is noteworthy that nystagmus that occurs only on extreme lateral gaze is not pathologic because it occurs in 60% of normal people. [24]
Funduscopic: Papilledema or a loss of venous pulsations can denote increased intracranial pressure. Also, assess for optic neuritis.
Corneal reflex: Assess CN V (sensory) and VII (motor).
Mouth/Throat: Assess gag reflex. Determine asymmetry of tongue on protrusion.
Neck: Auscultate for bruits along the carotid artery from the supraclavicular fossa to the base of the skull. Determine whether neck movement aggravates or improves NVD. Palpate for an enlarged thyroid.
Lungs: Adventitious lung sounds may imply causes for hypoxia.
Heart: Special attention should be directed at determining the presence of valvular heart disease (especially aortic stenosis) and arrhythmias.
Rectal: Determine if stool is melanic in appearance or if guaiac positive.
Cranial Nerves: Cranial nerves should be specifically tested because the patterns may suggest both specific disease processes as well as areas of involvement. Any cranial nerve abnormality in combination with VD or NVD should be considered a sign of brain damage until proven otherwise.
The cranial nerves can be quickly and easily examined during the general head and neck examination. Olfaction and visual fields are not usually tested in the ED but should be if there are specific complaints in the history that suggest their involvement. Test direct and consensual pupillary constriction (II and parasympathetics via III), and the corneal reflex (Sensory V and motor VII).
Nystagmus is the observed movement of the eye in response to stimulation of the vestibular labyrinth, retrocochlear pathways, or central vestibulo-ocular pathways. For the purposes of this article, vertigo is a subjective symptom that correlates with the examiner’s objective observation of nystagmus. With the eyes open, the patient sees the environment move; with the eyes closed, the patient feels that he or she is turning or whirling in space. Because the only objective sign of vertigo is nystagmus, the emergency physician should be very thorough about evaluating nystagmus. Nystagmus is particularly valuable because it is generally not performance dependent, as are tests of balance and coordination.
There are two components to nystagmus: slow and fast. The slow component is caused by vestibular stimulation and is mediated through the three-neuron arc from the semicircular canals to the extraocular muscles. The fast component returns eyes to the resting position and requires a functioning cerebral cortex. As a result, the fast component will not be present in coma or under general anesthesia. Test for nystagmus in the primary gaze by having the patient fix on your finger. Then have the patient follow your finger through the range of horizontal and vertical gaze. Nystagmus also can be observed by asking the patient to look 45° to the left and to the right. If nystagmus develops, record the fast-phase and slow-down phase direction and the position in which they occur.
There are many types of nystagmus, and many authorities think that this is best evaluated quantitatively by electronystagmography (ENG). This is not practical in the ED because it is not easily accessible, however. ENG is an uncomfortable procedure, and most patients can be diagnosed without it. All that is needed in the ED is a clinical evaluation of nystagmus, because the important differentiation is whether the nystagmus is central or peripheral in origin. Central nystagmus can occur in any direction, although vertical nystagmus is always central. There is no relation between the direction of central nystagmus and the location of the lesion, and dissociation of movements between eyes is possible and can persist for years. As a rule of thumb, the following types of nystagmus are indicative of a central origin: pure vertical nystagmus, very active nystagmus without vertigo, direction changing/unipositional nystagmus, gaze paretic nystagmus, disconjugate eye movement in nystagmus, and failure of fixed suppression in acquired nystagmus. [1] [52]
Peripheral nystagmus is usually horizontal, with a rotary component, and the fast component points away from the affected side. Peripheral nystagmus generally lasts only minutes to weeks. Rotary nystagmus is very common with peripheral VD.
Special attention should be paid to assessing the corneal reflex (sensory V and motor VII). A decreased corneal reflex in the setting of VD may indicate an acoustic neuroma.
All three motor divisions of CN VII should be tested because peripheral lesions cause complete paralysis over an entire side, whereas central lesions leave the forehead intact owing to crossover ( central sparing or forehead sparing.)
In the setting of vertigo, CN VIII is the most important CN to test because of its vestibular and cochlear components. These two nerves are very close to one another, and because of their proximity a disease process of one may affect the other. The vestibular portion of CN VIII has been discussed previously (in the nystagmus section). The cochlear portion of CN VIII is responsible for hearing. To assess the cochlear system properly, one must determine the presence of a pure tone hearing loss.
The emergency physician should bear in mind that there are three general types of deafness: conductive deafness, sensorineural deafness, and central deafness. Conductive deafness is due to a defect in the mechanism by which sound is transformed and conducted to the cochlea. Prime examples of conductive deafness include the various disorders of the external or middle ear. Sensorineural deafness is due to disease of the cochlea or of the cochlear division of the eighth cranial nerve. Central deafness is due to lesions of the cochlear nuclei and their connections with the primary receptive areas for hearing in the temporal lobes.
The two peripheral forms of deafness, conductive and sensorineural, must be distinguished to arrive at an effective treatment plan. In differentiating sensorineural from conductive deafness, tuning fork tests are often used because of their accessability and inexpensive cost. Preferably, a 512-Hz frequency vibrating tuning fork is held about 2.5 cm from the ear to test for air conduction. Sound waves will be heard only as they are transmitted through the middle ear. If there is a disease or lesion in the middle or external ear, then the sound waves will be reduced or not appreciated at all. When the vibrating tuning fork is applied to the skull to assess bone conduction, the sound waves are conveyed directly to the cochlea. The status of the sound transmission apparatus of the middle ear is bypassed. Normally, air conduction is better than bone conduction.
The Weber test assesses the presence or absence of a sensorineural hearing loss. In the Weber test, the vibrating tuning fork is applied to the midline of the forehead. A normal person hears the sound equally in both ears. In sensorineural deafness, the sound is localized or best heard in the normal ear, whereas in conductive deafness, the sound is localized in the affected ear.
The Rinne test evaluates for a conductive hearing loss. In fact, the Rinne test is really a comparison of the patient’s hearing sensitivity by bone conduction with that by air conduction. The Rinne test is carried out by first placing the handle of the struck tuning fork, on the mastoid process and, then, beside or lateral to the ear. The tuning fork placed against the mastoid process elicits bone conduction, whereas the tuning fork is held beside or lateral to the ear generates air conduction. If the sound is heard best when the handle is held against the mastoid process, a conductive hearing deficit is present and implies a lesion in the middle ear. If the sound is heard best when the tuning fork is placed beside the ear, either the hearing is normal or a neurosensory hearing loss is present. In summary, bone conduction is heard better than air conduction in patients with conductive hearing loss. Conversely, patients with normal or neurosensory hearing loss perceive air-conducted sound better than bone-conducted sound. [1]
Cerebellum: No neurologic examination is complete without evaluating the patient’s ability to stand and walk. An abnormality of stance or gait may provide diagnostic clues to the cause of the dizziness.
Provocative Physical Tests (Diagnostic Physical Adjuncts):
The performance of provocative physical tests can be extremely helpful to the emergency physician because they help to elicit subjective symptoms, clarify the complaint, facilitate the diagnosis, and cost nothing but the physician’s time. The test results are considered positive if the symptoms are reproduced.
If the patient gives a history of NVD, the emergency physician should perform the following provocative tests:
Orthostatic vital signs: A positive test result indicates decreased cerebral perfusion, with considerations including orthostatic hypotension, anemia, and volume depletion.
Hyperventilation for 3 minutes: A positive test result suggests anxiety or psychogenic causes. [11]
Valsalva’s maneuver for 15 seconds: A positive test result implies a cardiac origin, such as aortic stenosis or other valvular lesions.
Carotid sinus stimulation. A positive test result indicates a hypersensitive carotid sinus with either a cardioinhibitory or a cardioaccelatory response. It is noteworthy that this test should not be performed in patients with known or suspected carotid vascular disease or in elderly patients. [44]
If the patient gives a history of VD, then the following provocative tests should be considered:
Nylen-Barany (Hallpike-Dix) Maneuver: This maneuver should be part of the physical examination in every patient that complains of vertigo because it helps to identify a peripheral or positional component to vertigo. In this maneuver, the patient is seated on a flat examination table with the head rotated 45° to one side. The patient is then moved backwards into a lying position, with the head still deviated and hanging over the side of the table. Nystagmus as a result of peripheral vertigo begins within 30 seconds of completion of this maneuver and lasts less than 30 seconds. If nystagmus persists while the patient is in this position but is not present while the patient is sitting, a central vestibular lesion is probably the cause of the patient’s vertigo.
Vestibulo-ocular reflex (VOR): This is a simple test that can be performed at the bedside and is used to determine whether or not the vertigo is vestibular in origin. By means of the VOR, a movement of the eyes is produced that is equal and opposite to the movement of the head. The VOR is mainly a response to rapid transient head movements. The VOR be assessed at the bedside, even in patients with acute vertigo, providing that the clinician uses the head thrust test. The patient fixates on a target while the physician quickly moves the patient’s head approximately 15°. If the VOR is normal, the eyes will remain focused immediately on the target after the head is thrust. If the patient must make corrective eye movement to see the target, the VOR is decreased. Corrective eye movements (saccade) when the head is thrust to the left and right indicate vestibular dysfunction on the left and right sides, respectively. Other bedside tests of the VOR can be performed but require special equipment that may not be readily available. For example, the currently accepted gold standard for rotational testing of the VOR uses a servocontrolled chair for sinusoidal whole-body rotation.
Head-shaking Nystagmus: Head-shaking nystagmus is defined as the nystagmus that appears after vigorous horizontal head shaking for about 15 seconds, at a frequency of approximately 2 Hz. The phenomenon of head-shaking nystagmus is conventionally thought to occur when differences in peripheral vestibular input ultimately reach the postulated region of the central velocity storage mechanism of the brain stem. A positive head-shake test result suggests a peripheral lesion.
Walking with sudden turns: This test produces veering toward the side of cerebellar or labyrinthine disease. The patient should actually pivot on a given point on the ground.E. Valsalva’s maneuver for 15 seconds: A positive test result may indicate a posterior fossa lesion or a perilymphatic fistula.
Fukada stepping test: This test is performed by marching in place with eyes closed for 50 steps at normal walking speed. A positive test result indicates VD. The examiner should pay special attention to body sway, changes in head position relative to the body, and position of the arms in horizontal or vertical directions. The final position is regarded as abnormal if there is more than 30° of body rotation or more than 1 m of displacement from the starting point.
Fistula testing: Fistula testing is an effort to mobilize labyrinthine fluids by alternately generating an increase and decrease in the air pressure of the external auditory canal. The patient’s head is tilted 60° in extension while a pneumatic otoscope is used with an occlusive fit. A positive test result is when positive pressure elicits vertigo and nystagmus. The commonest cause of a positive fistula test is a cholesteatoma. If the patient has a labyrinthine or perilymphatic fistula, the eyes will deviate to the right and left with alternating positive and negative pressures. [19]

Laboratory Tests

Historically, the standard of care for managing dizziness included a large battery of laboratory tests–regardless of the history and physical. In 1991, the medical care costs for managing patients with dizziness exceeded $1 billion. [33] Deducing certain findings on laboratory tests may help to confirm a suspected diagnosis; however, not all patients require such testing, and a shotgun approach to testing is not cost effective. In the days of managed health care, limiting


expensive and low-yield laboratory tests is of the utmost importance. Most causes of dizziness can be determined by a complete patient history and physical examination.

For example, the patient experiencing VD should not require much, if any, laboratory testing to arrive at a diagnosis, because VD is usually an anatomic and generally not a metabolic diagnosis. Metabolic causes for true vertigo include drug toxicity, hypoglycemia, and hypothyroidism. Hypoglycemia should be considered in any diabetic patient with vertigo. The lesion that is causing the VD symptoms should be defined primarily by physical examination. The real question for the clinician in this scenario is whether a neuroimaging study will better define the lesion.

The patient with NVD may benefit from a limited or restricted laboratory evaluation consisting of a CBC and a basic metabolic panel (Chem-7). A pregnancy test may be indicated in women of childbearing years. For most patients, this limited amount of laboratory will provide the diagnostic answer. A more comprehensive metabolic panel can be obtained, but many of the laboratory results will not be beneficial, the results will not be readily available, and the tests will be expensive. Additional diagnostic tests to consider include a thyroid profile, serologic test for syphilis (RPR or VDRL), urinary drug screen, and drug levels. The rationale for ordering these or any diagnostic studies is to confirm the initial assessment based on the history and physical examination, and not to exclude a laundry list of rule outs.

From the patient history, if a cardiovascular etiology is entertained, an ECG to evaluate for the presence of a myocardial infarction, a cardiac arrhythmia, or a heart block is indicated. Placing the patient on a cardiac monitor may assist the clinician in capturing a transient or intermittent arrhythmia.
Radiographic Imaging

Not all dizzy patients require an imaging study. If the patient is dizzy but has no abnormalities on careful examination, then no imaging studies are indicated. The patient with NVD will ultimately be given a nonanatomic or metabolic diagnosis, and no neuroimaging studies are indicated. If abnormalities are detected on examination that suggest CNS disease or invasive otologic disease, imaging should be pursued as deemed appropriate. If history and physical examination are consistent with a specific peripheral vestibular diagnosis, Meniere’s disease, or benign positional vertigo, then there is no need for imaging studies. In cases of acute VD, if the patient is at high risk for cerebrovascular disease by virtue of age and additional risk factors (usually presenting with central VD), imaging should be pursued. [15]

If a neuroimaging study is indicated, the question arises whether to order a CT scan or a MRI. The answer is found in two parts: 1) is MRI readily accessible and available? and 2) what are the clinical concerns or differential diagnosis? If the clinical concern is an acute intracranial hemorrhage, then a CT scan of the brain will suffice; however, a low-resolution head CT scan without enhancement plays little role in the evaluation of the patient with dizziness. If there is concern about the possibility of a cerebral infarction or a tumor (especially of the posterior fossa) then an MRI is the imaging study of choice because CT scanning lacks the sensitivity of MRI scans for investigating cerebral infarctions and tumors of the posterior fossa. Accordingly, MRI is the most sensitive test to rule out an acoustic neuroma. From this perspective, it should be obvious that imaging studies should be ordered based on the detection of abnormal neurologic signs. [25]


The most useful diagnostic approach is to determine whether the patient’s complaints arise from an inner ear (labyrinthine) problem, a brain lesion, both, or neither. Patients having inner ear or brain pathology usually present with true vertigo and will be considered to have VD. Patients having metabolic, cardiac, respiratory or some other systemic disorder generally present with diffuse weakness or a sensation of lightheadedness and will be considered to have NVD.
Central Versus Peripheral Vertigo

In the evaluation of true vertigo, it is important to make the differentiation between peripheral (vestibular) disorders and CNS disorders. Peripheral disorders commonly have disabling symptoms, such as vertigo and vomiting, but are rarely life threatening. Central vertigo may be insidious in onset and produce mild symptoms but can be indicative of progressive CNS dysfunction. Both the symptom (vertigo) and the sign (nystagmus) have characteristic features that indicate peripheral or central causes. As previously discussed, the physical sign of nystagmus has distinctive features that help to differentiate between peripheral and central causes. Peripheral nystagmus is usually horizontal and has a rotary component. Additionally, peripheral nystagmus is only minutes to weeks in duration, and the fast component points away from the affected side. In contradistinction, central vertigo can occur in any direction, and dissociation of movements between the eyes is possible. [20] Furthermore, in central nystagmus there is no relation between the direction of the nystagmus and the location of the lesion. Vertical nystagmus is always central in location. Surprisingly, central nystagmus may be present for years. [30]
Examples of Peripheral Vertigo

Some of the commoner causes of peripheral vertigo are benign positional vertigo, labyrinthitis, vestibular neuronitis, motion sickness, Meniere’s disease, peripheral vestibulopathy, and acoustic neuroma. A rare but classic cause for peripheral vertigo is a perilymphatic fistula.
Examples of Central Vertigo

Although central vertigo is not as common as peripheral vertigo, its clinical significance is more decisive and often critical. Some of the disease processes that present with a central vertigo are upper and lower brain stem lesions, basilar artery migraines, vertebrobasilar ischemia or infarctions, multiple sclerosis, acute cerebellar lesions (hemorrhage or infarction), cerebellopontine tumors, and dysfunction of vestibular portion of CN VIII. Rarely, seizures and spinocerebellar degeneration will present as central vertigo.

Nonvestibular (Nonvertiginous) Vertigo

The differential diagnosis for NVD mostly includes any disease or disorder that results in inadequate cerebral perfusion (Table 1) . Attention should be paid to disease processes within the following organ systems: cardiac, metabolic/endocrine, gastrointestinal, obstetric/gynecologic, pulmonary, and vascular. Special consideration should be given to any infection, prescribed drug, or illicit drug as the causal agent for the NVD. Psychogenic disorders should also be considered, as should the many causes of orthostatic hypotension.


The common denominator with respect to treatment of NVD is to identify and manage the underlying cause. If the responsible disease or injury results in decreased cerebral perfusion pressure, efforts should be made to increase the cerebral blood flow. This may require the use of intravenous fluids, blood transfusions, cardiovascular stabilization, oxygenation, or the removal of the causal drug. Accordingly, hospitalization may be necessary to manage the underlying cause adequately. If the NVD is psychogenic in origin, moral support or the demonstration of concern for the patient is also very important–even if the patient has had the dizziness for years. Referral to a mental health clinic may provide definitive care.

Because most causes of vertigo are peripheral (85%) and not life threatening, the primary therapeutic goal is to provide symptomatic relief from the vertigo as well as the nausea and vomiting. Several different medications are available to aid treatment. A key factor that determines which drug will be used is based on the degree of sedation that is desired. Meclizine is the most commonly used agent to suppress these symptoms and displays only mild sedative effects. Dimenhydrinate and diphenhydramine are ethanolamines, equally effective, and are more sedating than meclizine. Scopolamine, available again in the transdermal form after withdrawal from the market, is considered to be the most effective treatment for motion sickness but is not effective for labyrinthine disease. Also, caution should be used in elderly patients because of side effects of confusion, hallucinations, and memory loss. Intramuscular promethazine immediately relieves the symptoms of space motion sickness in 90% of patients. [14] Diazepam is the most potent vestibular suppressant but causes significant sedation and has the potential for abuse.


Most patients that present to the ED with dizziness can be discharged safely to home care and be treated appropriately on an outpatient basis. The onus on the emergency physician is to identify the few dizzy patients who actually warrant admission to the hospital. A general rule of thumb that one can use is that all patients with central VD should be hospitalized. The lesions or diseases that present as central VD are significant, debilitating, and often life threatening. The patients with peripheral VD can usually be managed on an outpatient basis with supportive care. Extenuating circumstances such as intractable nausea and vomiting, volume depletion, and poor social support at home justify admission to the hospital. The acute onset of peripheral VD can be very debilitating, and patients with it should be confined to bed. If there is no one at home to assist in the patient to eat or get to the bathroom, then hospitalization is recommended; the elderly are particularly at risk for falling and injuring themselves under such circumstances.

The disposition of patients with NVD was discussed previously. If the clinical concern is of cardiovascular, metabolic, pulmonary disease, systemic illness, or CNS infection, a minimum of a short stay (23-hour observation) would be prudent. The causes for orthostatic hypotension are extensive, and the decision for admission should be based on the prognosis as well as social support mechanisms. In general, most patients with NVD can be sent home with follow-up care by their primary care physician.


One of the most challenging patients in the ED is the child or infant with dizziness. Dizziness is a nonspecific complaint that is used to describe a variety of symptoms with completely different pathophysiologic mechanisms. Children with the sensation of vertigo, light-headedness, near-syncope, disequilibrium, or visual disturbances can present with dizziness. In evaluating patients with dizziness, the history is the most helpful aspect in arriving at a diagnosis. Unfortunately, the difficulty in obtaining a history from young children makes the evaluation of dizziness very difficult. Furthermore, infants with dizziness can present with nonspecific symptoms, such as vomiting, pallor, or crying, with few physical findings suggesting dizziness as the cause of their symptoms. Often the physician must rely on parents and family members to obtain a history, which has significant limitations when evaluating a subjective complaint such as dizziness. Because many emergency physicians rarely see pediatric patients with dizziness and have difficulty obtaining a history from the patient, this complaint often is either ignored or a shotgun approach is taken, with a large battery of laboratory tests ordered that usually yield normal results and often are not helpful in evaluating the dizzy child.

The definition of dizziness in pediatric patient does not differ from adults. Body equilibrium is maintained through the integration of three systems: the vestibular, visual, and proprioceptive systems. When any of these systems or their brain stem connections are impaired, dizziness may result. Although the neural pathways of these three systems are not fully developed at birth, they are fully myelinated and completely developed by the age of 4 months. [27] Thus, vertigo (defined earlier a type of dizziness in which there is an abnormal sense of motion in which is usually a spinning sensation) can occur even in infants. Vertigo is usually the result of dysfunction of the vestibular system. The vestibular system is among the first of the CNS projections to function in infancy because there is clear evidence through reflex responses to movement and positional changes that the vestibular system is functioning within the first 6 weeks of life and is completely developed by 16 weeks. [37]

As discussed earlier, dizziness is a very common complaint in adults; however, it is unusual in the pediatric population. There have been few studies on the incidence of dizziness in pediatric patients. In one study to determine the frequency of dizziness as a primary complaint in children, the medical records of all pediatric patients admitted to Boston City hospital over a 12-month period were reviewed to determine the number who presented with dizziness. Of the 2,088 pediatric patients admitted, 238 patients had a discharge diagnosis related to the balance mechanism. Only 14 of these 238 patients had a presenting chief complaint of dizziness. [32] Because most pediatric patients that present with dizziness have a benign, self-limited disorder, this study population, which included only patients admitted to the hospital, may not be representative of the actual incidence of dizziness presenting to the Emergency Department. Although most children with dizziness have benign disorders, the symptoms can be very distressing to the patient and the parents. The physician must also remember that dizziness can be the initial symptom of serious or life-threatening disease. Thus, every pediatric patient complaining of dizziness warrants careful evaluation. A diagnosis usually can be established with a thorough history and examination and few ancillary tests. This section reviews the important aspects in the history and examination, the differential diagnosis, work-up, treatment, and disposition of the pediatric patient presenting with dizziness.
Important Historical Features

The history is the most important element of evaluating the child with dizziness. A good history will significantly narrow the differential diagnosis and will direct the emergency physician which further tests (if any) are needed to confirm a diagnosis. The first aspect of the history is to try to determine if the complaint of dizziness is truly vertigo or is nonvertiginous in nature. This can be difficult in the young child, but even children as young as 4 to 5 years of age can give good descriptions of their symptoms when asked. The presence of true vertigo in infants or children less than 3 years old is difficult to establish, but several aspects of the history can indicate true vertigo. Episodic periods of ataxia, irritability, or vomiting associated with nystagmus observed by the parents strongly suggests vertigo. If the patient appears to have true vertigo, the differential diagnosis can be narrowed to disease that affect the vestibular system (centrally or peripherally), with the exception of a few miscellaneous nonvestibular processes that can cause vertigo.

In children with vertigo, several historical features are helpful in determining a proper diagnosis. The presence of ear symptoms, including tinnitus, hearing loss, or recurrent ear infections, will help to direct work-up of the disease. The presence of nystagmus is also helpful. The general level of consciousness of the child during and after attack is important. Any alterations of consciousness suggests the possibility of seizure, which is a relatively common cause of vertigo in children. Associated features such as headache and flashing lights can suggest basilar artery migraine as the cause. Recent or remote head trauma is also important, and this information may not be reported in situations of child abuse. The characterization of symptoms is also important to differentiate between a central or peripheral cause. Sudden intermittent severe attacks are more indicative of a peripheral process, whereas chronic progressive vertigo that is less disabling is typical of central causes. [22] [27]

Family history is important because several causes of vertigo in children have a strong hereditary component. One study of eight children with basilar migraine headaches associated with ataxia and vertigo showed that seven of the children had a striking family history of migraine headaches, with most of the affected members being female. A family history of hearing loss, vertigo, or seizures also should be obtained. One study of 25 children with vertiginous seizures showed that 13 had a positive family history of seizures and 5 had a history of a previous febrile seizure in infancy. A history of previous use of ototoxic drugs is important. The aminoglycosides, furosemide (Lasix), quinine, ethacrynic acid, salicylates, isoniazid, phenytoin, and carbamazepine are common pharmacologic causes of vestibular dysfunction and vertigo. Illicit or street drugs also can cause vertigo. A history of perinatal infections, especially those children having had the TORCH diseases, should be investigated. [2] [6]

Pediatric patients with nonvertiginous dizziness are more likely to have symptoms from a systemic disorder than those with vertigo. Again, the severity, onset, and timing of symptoms should be obtained. The activities during symptoms should be noted because dizziness with exertion can occur with cardiac disease, and dizziness with orthostatic maneuvers can be evidence of volume depletion, anemia, or autonomic nervous system dysfunction. A careful review of systems can help to direct the physician to a probable cause. Associated chest pain, shortness of breath, or palpitations can be associated with cardiac disease. Fever can point towards an infectious origin. Polyuria and polydipsia may indicate undiagnosed diabetes. Medical and family history should be evaluated for the presence of diabetes, thyroid disease, anemias, cardiac disease, hypoglycemia, and Addison’s disease. Dizziness can also be a symptom of depression and anxiety, so that information about social stressors such as school and family situations should be obtained. Important historical features in evaluating the child with dizziness are summarized in Table 2 .
Physical Examination

A thorough physical examination should be done, with special focus on the ENT, cardiac, and neurologic systems (Table 3) . The examination should begin with the general appearance of the child and vital signs. Hypotension and tachycardia may suggest volume depletion, sepsis, anemia, dysrhythmia or cardiac disease. Hypertension also can reflect cardiovascular disease. Again, one area of the physical examination that is of special interest is the ears, as abnormalities of the ears are a common cause of dizziness in children. The ear examination should focus on signs of otitis media, middle ear effusion, or a foreign body in the external auditory canal. Postauricular swelling, tenderness, or induration suggests mastoiditis or suppurative labyrinthitis. Informal testing of hearing can be done at the bedside, as can Weber’s and Rinne’s tests for conduction and sensory hearing loss in cooperative children. Fistula testing (to elicit Hennebert’s sign) should be done in patients suspected of having a perilymphatic fistula. This test is done by applying positive and negative pressure to the external canal through the use of pneumatic otoscopy. The presence of induced nystagmus or subjective dizziness is suggestive of a perilymphatic fistula. [6] Evidence of congenital anomalies such as malformation of the external ears, hypopigmentation, or craniofacial dystosis should be noted, as should evidence of trauma to the head or neck. Auscultation of the neck for bruits and the presence of lymphadenopathy or tenderness should be noted. Cardiac auscultation for abnormal murmurs and palpation of peripheral pulses should be done to look for congenital cardiovascular disease.

A careful neurologic examination should be done in all patients with dizziness. Much of information can be obtained simply by observing the child’s actions, play, and reflex behavior. In general, children over the age of 4 years will cooperate for a full neurologic examination similar to that performed in an adult. Obviously, children under the age of 4 years are unlikely to cooperate with detailed neurologic examinations, thus more information is obtained through observation of play, developmental actions, and reflexes.

In older cooperative children, testing of cranial nerves, visual fields, and the observation of spontaneous nystagmus is important. Cranial nerve deficits suggests a brain stem tumor. The presence of nystagmus should be noted, including the direction and character of the nystagmus. Peripheral vestibular lesions cause a jerk nystagmus, with the slow component toward the affected side. Central or cerebellar lesions cause nystagmus with the quick component toward the affected side, and a reversal in the direction of the fast component when changing from right to left lateral gaze. Vertical or rotary nystagmus also suggests a central origin. [32] Testing of general muscle tone, strength, and tendon reflexes should be done to assess for abnormalities of the pyramidal tract. Cerebellar and vestibular function can be tested by tandem gait, hopping, and toe-to-heel gait, with eyes opened and close. An abnormal gait can be the result of cerebellar or acute vestibular disease. Children with chronic vestibular disease are generally able to compensate for their vestibular dysfunction through the use of visual cues, and thus will have no abnormalities of tandem gait with their eyes opened. Those with cerebellar disease are impaired with eyes opened or closed. The Romberg test is also helpful in evaluating vestibular dysfunction. The Romberg test is done by having the patient stand with feet together and eyes closed. A positive Romberg test is seen when the patient falls to one side, and is indicative of vestibular dysfunction or loss of position sense. With vestibular disease, the patient will fall to the side of the affected labyrinth. Patients with acute vestibular dysfunction cannot maintain position during a Romberg test; however, those with chronic vestibular disease are able to compensate and maintain normal position. To test for subtle chronic vestibular dysfunction, a tandem Romberg test should be done, in which Romberg test is done with one foot in front of the other. Normal children are able to maintain this position for at least 5 seconds. This is a more sensitive test for vestibular dysfunction, and the patient will again fall in the direction of the affected labyrinth. [17] [32] The stepping test can also help detect vestibular abnormalities; it is performed by having the child step in place with his or her eyes closed for 60 seconds. Deviation from the initial direction in which the child was facing of more that 45° to the right or left indicated vestibular dysfunction on the side of the deviation. [6]

The Nylen-Barany (Hallpike-Dix) test can be performed at bedside in cooperative older children. This is done by having the patient sit upright, with the head rotated 45° to one side. The patient is then quickly moved from the sitting position backwards into a lying position, with the head still rotated and hanging over the side of the bed. The eyes are observed for nystagmus, noting the time of onset, duration, and direction of the nystagmus. The patient is also queried for symptoms of vertigo with the maneuver. The maneuver is then repeated from the sitting position to the other side. The presence of nystagmus with this test indicates vestibular dysfunction, and certain features of the nystagmus and symptoms suggests a peripheral or central cause. Central processes typically cause immediate nystagmus that is not subject to adaptation or fatigue with repetition of the maneuver, and the patient is usually only mildly symptomatic. Peripheral processes cause intense nystagmus that develops 20 to 30 seconds after the maneuver and is characterized by rapid adaptation and resolution of the nystagmus with repetitive maneuvers. With peripheral vestibular disease, the patient is usually intensely vertiginous with the Hallpike-Dix maneuver. [32] [50]

As mentioned, specific testing for vestibular disease is difficult in uncooperative young patients and in infants. There are, however, several rough maneuvers to assess for vestibular function in infants. Induced nystagmus with head movement can generally be seen even in infants, when present. The vertical acceleration test can be done to assess vestibular function in infants; this test consists of holding the baby in the supine position at arms length with the head aligned with the body. The examiner then abruptly descends to a semicrouched position, providing vertical acceleration to the labyrinth of the infant. The normal response is abduction and extension of the upper extremities followed by an embrace, which indicates normal vestibular function. [18] The most primitive form of labyrinthine reactions, the tonic neck reflexes, can be tested in infants by rotating the head, which causes angular acceleration to the labyrinths. The normal response is a tonic reaction of the extremities, which indicates integrity of the vestibular and pyramidal tract systems. [17]

After completing a thorough history and examination, the emergency physician should be able to generate a differential diagnosis, with selective use of imaging and ancillary studies to help confirm the diagnosis, or at least to rule out a potential life-threatening disorder.
Differential Diagnosis

The differential diagnosis of pediatric dizziness is extremely large (Table 4) , but the emergency physician should be able to narrow the differential diagnosis extensively by a good history and physical examination. It is easiest to attempt to differentiate true vertigo from nonvertiginous dizziness because the pathophysiology of each is different and narrows the differential diagnosis substantially. If the patient has true vertigo, differentiating between peripheral and central vestibular disease will help to narrow the differential even further.


Magnesium for Migraines?

By: | Post date: February 23, 2017 | Comments: No Comments
Posted in categories: Health

Over 24 million people in the US suffer with migraine headaches.  If your one of those people, you know how difficult it is to find something that works.  Magnesium works!!  After 22 years of suffering with migraines, I am now painfree with the use of Magnesium supplements.  This is what prompted me to create this website.   

Magnesium works as a natural calcium channel blocker and a smooth muscle relaxant.  It is a mineral that is normally found in our bodies and researchers have found that during an acute migraine attack, our Mg levels are lower than normal.  In these studies they treated their patients with IV Mg during an acute attack and found that over 80% of their patients got complete relief of their migraine.  

On this site we have information to help you learn more about the use of Magnesium for your migraines.  The first thing you need to learn is how to dose yourself.  Just running to the drugstore and picking up any Mg product and taking one in the morning will not work!  You need to read about the various Mg salts and how they work, how to dose with these products.  If you do this you will have success.  No its not a miracle cure!  But it will decrease the number of migraines that you get and those that you do get will decrease in intensity.  Over time many people find their migraines go away completely.  

No I don’t work for a pharmaceutical company and have no investments in any one particular product.  The information provided on this site is from my own personal experience and from researching information on the various Mg salts.  So its not a sales pitch for Magnesium.  I just found that it worked for me and over the past year has worked for many people who have visited this site.  You can stop in the Migraine forum if you have any questions.  The people who have had success with Magnesium also post there and can help you by sharing their experiences.  So visit the pages I have provided on this site to learn more about Mg, headaches, medications and more.  Then stop in the forums or email me if you have any questions about your specific case.  I hope you find yourself painfree soon!