SENSORY CONFLICT AND OTHER CAUSES OF DIZZINESS: ETIOLOGY, DIFFERENTIAL DIAGNOSIS, AND MANAGEMENT(a)


Robert L. Yolton, OD, PhD

Pacific University College of Optometry

COPE Certification 13539-SD Expires 04/01/2008

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INTRODUCTION

"Doctor, sometimes I feel really dizzy" is a complaint occasionally heard during optometric examinations. A 1985 nationwide survey found that for patients over 25 years of age, dizziness accounted for 1% of all chief complaints presented to primary care providers.(1) In terms of management, 1.5% of patients with this complaint were admitted to a hospital, 4.4% were referred to a specialist, and 89% were prescribed medication.(1)

Dizziness becomes a greater problem as patients get older. In the elderly, almost one out of five reports dizziness that impairs daily activities or is severe enough to warrant medical attention.(1,2) In patients over the age of 75, dizziness is the most common complaint made to primary care physicians.(3) Given the frequency of the problem, it is not surprising that optometrists often encounter complaints of dizziness.

Typically, optometric management of dizziness involves an evaluation of the patient's refractive, binocular, accommodative, and visual status. If this examination is not productive, the patient is usually referred to a family care physician. The physician will probably treat the dizziness with a symptom suppressing medication or might send the patient on to a specialist in an attempt to discover the cause of the problem.

In this paper, the various distinct sensations that are usually referred to by patients as dizziness will be reviewed, the causes of these sensations will be discussed, and management plans associated with some of the etiologies will be presented.

What is Dizziness?
Patients typically define almost any state involving loss of normal mental processing as "dizziness." For diagnostic purposes, however, it is very important to obtain complete and accurate information regarding exactly what the patient experiences when they are dizzy. Symptoms will be described somewhat differently by each patient, but generally they can be classified into one of four categories: vertigo, near-syncope, disequilibrium, or ill-defined lightheadedness.(4) (Sometimes vertigo is considered to be a separate diagnostic classification, and the latter three problems are grouped together under the heading of "pseudo-vertigo," but it is useful to consider them independently.)

Careful classification of the patient's symptoms is important because it helps to determine a diagnosis and management plan. For this reason, each of the classifications will be reviewed separately.

CLASSIFICATION OF DIZZINESS
Vertigo
Patients who experience an illusion of false motion between themselves and the outside world are classified as suffering from vertigo.(5-9) Patient complaints consistent with this diagnosis include "the room is spinning," "things are whirling," " I am reeling," "everything is swaying," "things are pitching," or "it looks like things are rocking."(10)

Patients who have vertigo share two attributes in common: they perceive illusory motion and they typically do not experience a loss of consciousness. The motion perceived by patients experiencing vertigo can either involve a perception that the world is moving while the body remains still, or that the body is moving while the world remains still. In the first case, the patient is said to be experiencing objective vertigo; in the second case, subjective vertigo.(6) Although different neural mechanisms might be involved in these two conditions, the type of vertigo the patient experiences is not believed to have specific diagnostic significance. In both cases, the vertigo probably results from a discrepancy between the brain's expectation of sensory inputs and the conflicting cues it receives from the vestibular, visual, and/or somatosensory systems.(7,11,12)

Vertigo, except for the very mildest forms, is usually accompanied by varying degrees of nausea, vomiting, pallor, and perspiration.(13) These signs and symptoms indicate excessive activity in the autonomic nervous system. The patient's gait can also become unsteady and walking might be difficult during an acute attack of vertigo. The sensations of false movement can be so intense that the patient could be forced to lie down, usually on one side, with the eyes closed.(13) Even the slightest motion can aggravate the disorientation, nausea, and vomiting, so patients with acute attacks of vertigo tend to remain very still.

Near-Syncope
Syncope (or fainting) is defined as a transient loss of consciousness usually caused by inadequate blood flow to the brain.(5,14,15) Near-syncope (sometimes called pre-syncope) involves the patient's perception that she or he is about to faint.(10) Specific signs and symptoms can include a sensation of buzzing in the head, rubbery legs, constriction of the visual field, pallor, sweating, and nausea. This condition differs from true syncope in that loss of conscious does not actually occur, but there is no qualitative difference between syncope and near-syncope with respect to the differential diagnosis.(16)

Commonly, patients who experience near-syncope refer to their symptoms as dizziness, but careful questioning can separate this sensation from the spinning or moving sensations associated with vertigo. Near-syncope usually occurs as acute attacks, but occasionally patients describe chronic problems.(17) The severity of the patient's symptoms depends on the magnitude of the blood flow reduction experienced by the brain.(5,16)

Disequilibrium
Disequilibrium involves the sensation of losing one's balance without a feeling of illusory movement or impending loss of consciousness.(5,10,10a) Unsteadiness, particularly during walking, is a hallmark of disequilibrium; patients do not typically report problems when sitting still or lying down.(4)

Patients who report that they feel unstable often widen their stances or brace themselves to compensate. Some patients, especially those with vestibular problems can experience "drop attacks" in which they suddenly fall to the floor with no loss consciousness or awareness. Most likely, the vestibular system has signaled that a sharp movement was detected and it commands the body to make a compensatory movement. However, since the earth did not really move, the result is a fall.

Disequilibrium usually occurs because of a disruption in the integration between the patient's sensory inputs and their motor outputs. In normal persons, the brain coordinates the visual, vestibular, cerebellar, and somatosensory processes to maintain a sense of equilibrium and balance. A dysfunction within any of these systems can create disequilibrium.(11,16,18)

Aging is significantly associated with the onset of disequilibrium because the ability of the nervous system to process sensory inputs and control the postural reflexes declines with advancing age.(11,19,20) The effects result from a widespread degeneration of the musculoskeletal, neuromuscular and sensory systems.(21) Disequilibrium-related gait disturbances in the elderly are particularly accentuated by unfamiliar surroundings, uneven ground, and/or dim light, so many older persons avoid these situations. Although disequilibrium is not uncommon in the elderly, this symptom in young patients suggests neurological disease.

A CLINICAL PEARL. PATIENTS WITH SENSORY CONFLICT PROBLEMS OR FRANK FAILURES OF THEIR BALANCE SYSTEMS OFTEN PUT A HAND ON THINGS (E.G., WALLS, CHAIRS, ETC.) AS THEY MOVE ABOUT. THIS IS CALLED "GROUNDING" AND IT GIVES THEM A SENSE OF STABILITY. JUST WATCHING PATIENTS MOVE ABOUT CAN PROVIDE INFORMATION ABOUT THEIR EQUILIBRIUM.

Ill-Defined Lightheadedness
Normal persons feel lightheaded from time to time. The sensation can involve components of vertigo, pre-syncope, and/or disequilibrium, but the key feature of ill-defined lightheadedness is that the sensations are quite mild. For example turning the head sharply to the side or standing up quickly can produce a transient sensation of lightheadedness.(22)

Patients often describe a vague feeling of not quite being all there. They might describe the sensation as having difficulty thinking clearly, or just a funny feeling. The term "cloudy sensorium" is often used as a professional equivalent of ill-defined light-headedness.

Most people ignore these common, everyday sensations, but, for some patients, they can become quite bothersome. This is particularly true for patients who become sensitized to them because of psychological problems associated with anxiety, or because of other disturbances that have previously caused acute attacks of dizziness. These patients often place themselves in a "hyper-vigilant" state during which they constantly monitor themselves for any signs of impending dizziness. This can cause them to exaggerate their reactions to normal changes in body function and can produce great psychological distress.(23)

Lightheadedness can be very vague and difficult to diagnose accurately because patients often have trouble describing their sensations. Stress reactions, anxiety, depression, hypochondriasis, and panic disorders can all have lightheadedness as a primary complaint.(11)

However, care must be taken not to dismiss ill-defined lightheadedness as "all in the patient's head," and therefore of little concern. It can be an early symptom of a serious physiological or psychological problem, and it can be associated with a significant reduction in the patient's quality of life.

Mental Processing Overload

Patients with cloudy sensorium and dissociation report that they can't think, feel spacey or unreal, and some actually report out of body sensations. To understand these problems, remember what you feel like when you have a cold or an allergy attack, and your head feels like it is packed with cotton. Then multiply by 10 or 100 and add the anxiety of not knowing why this is happening. Often these symptoms are associated with an overload of the brain's information processing system. This overload is usually caused by a vestibular problem but it can be caused by visual imbalances too. It is also seen in association with prescription (and other) drug use.

CLINICAL PEARL. PATIENTS WITH SOME TYPES OF DIZZINESS PROBLEMS OFTEN CANNOT READ AND WALK (OR THINK) AT THE SAME TIME. THESE PATIENTS MUST SIT OR LEAN ON A WALL WHEN THEY READ TO RELIEVE ENOUGH OF THE BALANCE PROBLEM TO OBTAIN SUFFICIENT MENTAL RESOURCES FOR READING.

Seizure

It is not uncommon for patients with certain types of seizures to complain about dizziness. Grand mal seizures are not hard to miss, but the actual diagnosis and management can be tricky. These patient are typically already under the care of a specialist and are on various anti-seizure medications (which they might hate). It is much more difficult to detect petit mal seizures. These "absence attacks" are not usually associated with motor activity, just a total attention loss. Like grand mal seizures, petit mal can be treated with medications.

Patients with seizures that are not under complete control typically have their driving licenses suspended so you might have to make a house call to treat their vision needs unless other transportation can be arranged.

Currently, first aid for patients experiencing a seizure is to simply prevent them from hurting themselves by striking hard objects and allowing the seizure to run its course. You must be sure that the patient not experiencing a life-threatening attack, so a call to the paramedics could be indicated.

ETIOLOGIES OF DIZZINESS

Accurate classification of the patient's symptoms often provides valuable clues to the etiology of the underlying problem. Figure 1 shows how such a classification system can be used to aid in determining the cause of a patient's dizziness. It is quite possible, however, for a patient to experience problems that fall into several different categories. For example, a patient with acute episodes of vertigo might produce enough vagal activity to develop near-syncope or syncope. For this reason, careful clinical evaluation is necessary to discover the actual cause of the patient's dizziness. It must also be kept in mind that patients can present with multiple, co-existing problems, and this greatly complicates the diagnostic process (e.g., a patient with a vestibular problem creating vertigo could easily become worried enough to create a significant psychological problem).


Figure 1. Dizziness categorization. Figure modified with permission from: Manual of neurology: diagnosis and therapy, 4th ed. Samuels, MA. Copyright 1991, Little Brown and Co., Boston MA.


Although there are many causes of dizziness, five major categories will be reviewed: sensory conflicts, psychological problems, blood flow disorders, pharmaceutical effects, and systemic disease (including aging). Of these causes, sensory conflicts will be discussed in greatest detail because they are most closely related to problems involving the visual system.

Sensory Conflicts

Sensory conflicts often produce dizziness, typically with a major vertigo component. Under normal circumstances, the brain compares inputs from all of its sensory systems to determine posture, position in space, and body movement. When the information from all of the systems agrees, there is no problem. But, when disagreement is noted, problems begin. Even in normal patients, these sensory disagreements can occur when riding in the back seat of a car or in an airplane.(24) This is because the vestibular system detects motion/acceleration, but the visual system sees only the inside of the vehicle which remains fixed in space with respect to the observer. Another example is viewing a wide screen movie in which the audience vicariously experiences flying a jet fighter. The visual system reports motion, but the vestibular apparatus does not.

For example, in an airplane your vestibular and muscle senses might tell you that you are going up and down, tipping over, hitting severe turbulence, about to crash, etc., but your visual system says that the walls of the airplane (which are really closing in on you) are not moving and neither is the seat in front of you (about 6 inches in front of you these days). This sets up a conflict which can result in dizziness, motion sickness, vertigo, panic, and other wonderful sensations.

In an aircraft, we understand why these sensations occur, but for some patients, the sensations occur either continuously or episodically without an external cause. Because they typically involve visual system information as part of the conflict (even though vision might be contributing normal information), these conditions are of interest to you as a vision care specialist. In addition you will need to know how to prescribe lenses for these patients and make appropriate referrals.

A side-effect of this sensory conflict is an excessive response by the autonomic nervous system. This causes the sweating, pallor, nausea, and vomiting experienced by patients with vertigo.(13,25) Dimenhydrinate (Dramamine®) and a number of other prescription and non-prescription antihistamines can control some of these symptoms, presumably by suppressing vestibular output and reducing the amount of conflicting information the brain must process.(26-28)

When vertigo is not associated with actual movement, peripheral sense organ problems account for about 85% of the cases, whereas central processing disorders account for only 15%.(29) (Central disorders refer to problems in the cerebellum, brain stem, or projections to parts of the cerebral cortex, especially the temporal lobe. Peripheral disorders refer to problems occurring at the end organs or in the peripheral nerves.(16))

Sleep Disturbances

Many dizzy patients report sleep disturbances such as restlessness, or frequent awakening. These symptoms do not seem related to dizziness until we understand that if vestibular problems are causing problems for the awake patient, these same "bogus" vestibular conflict signals are telling the sleeping patient that he or she is moving. This information can break through to a high enough mental level that it awakens the brain to deal with the "earthquake."

Vestibular System Problems

Vestibular Apparatus

The vestibular apparatus is located in the inner ear and consists of a network of tubes called the semicircular canals, and a sac-like structure called the vestibule. This apparatus is filled with a small amount of fluid called endolymph and is surrounded by a second fluid called perilymph.(30) As the head moves, the inertia of the endolymph in the vestibular apparatus causes deformation of hair cells, and this results in the production of neural signals. These signals travel along the eighth nerve (the vestibulocochlear nerve) into the brain. The eighth nerve carries both auditory and vestibular axons, so it is common for patients with vestibular problems to also experience hearing anomalies. Also, because of the several reflexes that link eye movements to outputs from the vestibular system (e.g., the vestibular-ocular reflex), it is typical for patients with vestibular problems to report visual difficulties including nystagmus and shimmering of objects.(25,31)

Acute Inflammation of labyrinth

This condition typically occurs in patients between 30 and 60 years of age. For unknown reasons, the peak occurrence for females is in their 30's but for males it is in their 60's. It can be secondary to otitis media or meningitis. Symptoms include relatively sudden onset, acute vertigo, nausea, and inability to function. It is treated with antibiotics, antihistamines to quiet the inner ear, scopolamine, bed rest for a couple of days, and then increased activity to help the brain regain use of the vestibular information. The typical course of this condition runs about 6 weeks during which time the patient can be quite uncomfortable.

Perilymph Fistula

Several problems can cause the vestibular system to transmit faulty information. For example, trauma can cause mechanical damage to the vestibular apparatus or a more subtle problem called a perilymph fistula.(32,33) In the case of a fistula, perilymph leaks from the inner ear into the middle ear through a small hole in either the round or oval window membranes.(32) The result of this leakage can be a major alteration in the function of the vestibular apparatus with vertigo occurring as the brain attempts to process defective messages from the vestibular system. After an acute phase, the fistula can seal itself, but often it reopens intermittently as a result of exertion or changes in atmospheric pressure (e.g., flying in an airplane or a Valsalva maneuver such as during a cough or sneeze).(34) Treatment for this condition usually involves bed rest to encourage sealing of the fistula, or, in severe cases, an attempt can be made to patch the leak surgically.(30)

Endolymphatic Hydrops

Another problem that can cause the vestibular system to transmit faulty information is endolymphatic hydrops. In this condition, the pressure and/or electrolyte balance of the endolymphatic fluid inside the vestibular apparatus becomes unstable.(8) As a result, faulty signals are sent from the vestibular apparatus to the brain and this produces vertigo. Other signs and symptoms associated with hydrops can include hearing loss, tinnitus, and a sensation of fullness in the ears.

Pressure of the endolymph is maintained, in part, as a result of osmotic gradients between the endolymph, perilymph, and blood, so treatment is usually directed at stabilizing these relationships. Diuretics can be used for this purpose and hydrops patients are cautioned against upsetting their osmotic balance by consuming large quantities of salt, sugar, or alcohol. Some patients have found that they can self-medicate with these substances because their consumption temporarily reduces the endolymphatic pressure; unfortunately, the subsequent pressure rebound can greatly exacerbate their symptoms.

Hydrops patients often follow a chronic course with periods of greater and lesser symptom production (i.e., their symptoms can vary between mild disequilibrium and significant vertigo).(25) If symptoms become intolerable, a shunt can be surgically implanted to allow regulation of endolymph fluid pressure, or, if the symptoms become incapacitating, the vestibular apparatus and/or the eighth nerve can be partially or totally destroyed.

Ménières Disease

Ménières disease is a condition possibly related to hydrops. Both are thought to be related to changes in fluid pressure in the inner ear.(35) However, one of the major differences between Ménières and hydrops is that Ménières patients tend to experience severe, recurrent, acute episodes of vertigo whereas hydrops patients have problems that are often more chronic in nature.(11,13,16,25,29,34) Although the exact cause of these conditions is unknown, some have speculated that an allergy might be involved.(25) Therapy for Ménières is roughly the same as for hydrops including dietary restrictions, medication, and possible use of destructive procedures in severe cases.(36,37)

Infections

Viral or bacterial infections can also disrupt the function of the vestibular apparatus and cause the transmission of confusing information to the brain.(10,16) Normally, the inner ear is well protected against infections because it is sealed by its membranes against contact with the air, but bacterial middle ear infections (e.g., otitis media) can occasionally spread to the inner ear (possibly via a fistula) and produce labyrinthitis. It is also possible to have viral infections of the inner ear secondary to influenza and other systemic diseases.(8) Typically, inflammation of the inner ear will cause both vestibular and hearing problems with the vestibular problems manifesting as vertigo and nausea. Treatment of these problems relies on an accurate diagnosis and the use of appropriate antibiotics if the infection is bacterial.

Benign Paroxysmal Positional Vertigo

Although there are numerous other causes of vertigo related to vestibular function, one of the more common causes is benign paroxysmal positional vertigo (BPPV). This condition is also sometimes referred to as benign paroxysmal positional nystagmus (BPPN) because its occurrence is often accompanied by nystagmus. As its name implies, BPPV is a benign condition (i.e., typically not progressive or life threatening) that involves an acute sensation of vertigo occurring each time the head is moved in a certain direction.(8-10) The particular head movement that elicits the vertigo is different for different patients, but many BPPV patients have discovered for themselves what movement produces their symptoms.

As with many of the vestibular problems, the exact cause of BPPV is difficult to specify and may vary from patient to patient. Treatment can range from teaching the patient to avoid the movements that elicit the vertigo, to reassurance, and trial courses with anti-vertigo medications.

Detection of Peripheral Vestibular System Problems

Case History
Probably the most important method used to detect peripheral vestibular problems is a detailed case history including an exact statement of what the patient senses when they are "dizzy." It is imperative that the clinician allow the patient to verbalize their symptoms. Direct questions such as "do you feel as though you will fall?" should be avoided; patients will many times inaccurately respond yes. "What do you mean by dizzy?" is a better, open-ended question that will yield more beneficial information.(16)

It is also important to explore any history of trauma or illness, what conditions elicit the symptoms, what produces relief, and other physical anomalies that patient might have. A history of trauma can often be helpful in the diagnosis of fistula, specific head movements that elicit vertigo can help to diagnose BPPV, and other physical characteristics can help to diagnose syndromes that include vestibular disorders. An example of such a syndrome is the Waardenburg Syndrome. Patients with this syndrome have unusually wide-set eyes, cafe-au-lait spots, a white forelock, and inner ear problems that cause dizziness.(8,38)

Caloric Nystagmus
Often the reflexive interactions between the visual and vestibular systems can be used to aid in the diagnosis of peripheral vestibular problems. One of the most commonly used tests is caloric nystagmus in which the vestibular apparatus is warmed or cooled by the injection of fluid into the external auditory canal.(6,8) If the vestibular apparatus is functioning normally, a reflexive nystagmus is produced. The direction of this nystagmus is dependent on the ear being stimulated and on the fluid temperature. (When the fluid is cool, the nystagmus fast phase is in a direction opposite to the ear being stimulated, and when the fluid is warm, the fast phase is toward the ear. This relationship is associated with the acronym "COWS" - cold opposite, warm same.)(6,8) The acronym COWS holds when one ear is being stimulated but another acronym "CUWD" ( pronounced "CUD") is used when both ears are stimulated together. CUWD stands for cold-up and warm-down indicating the direction of the nystagmus fast phase beats.

Audiology
Because the peripheral vestibular and auditory systems share a common location, nerve, and fluids, vestibular problems are often associated with auditory difficulties. These hearing problems can range from an absolute or relative loss of ability to detect sound, to the false sensation of ringing or whistling sounds (i.e., tinnitus). These hearing problems can be monaural or binaural and can provide strong clues regarding the etiology of a patient's dizziness.(39)

Special Testing Procedures
Neuro-otologists and neurologists have developed a wide range of special testing procedures designed to diagnose vestibular problems. For example, electrocochleography is a technique in which a series of air pressure pulses is presented to the tympanic membrane and the resultant electrical responses from the cochlea are recorded.(40) Analysis of these responses can help in making a diagnosis of endolymphatic hydrops. Another example is electronystagmography which can be used to record the nystagmoid eye movements associated with a balance system anomaly.(41)

Clinicians also employ positional and rotational testing to diagnose vestibular dysfunction. Some of these procedures are the Nylen-Bárány maneuver, harmonic acceleration test, Romberg test and posturography.(8,11,15,16,30,41)

Other tests, such as measurement of brain stem potentials evoked by sound pulses, can also be helpful in detecting the auditory information processing problems that suggest vestibular or eighth nerve disease.(32,39)

Central Vestibular System Problems

Even if accurate information about movement, position in space, and acceleration is generated by the vestibular apparatus itself, the information can be garbled in transmission along the eighth nerve or can be misinterpreted within the brain itself. For example, a patient's symptoms of dizziness can be caused by one of the more common brain tumors: an acoustic neuroma.(8) This tumor grows along the course of the eighth nerve as it passes into the brain cavity, and can compromise information transmission in both the auditory and vestibular portions of the nerve. In addition, as the tumor grows into the cranium, it can compress the cerebellum and cause problems with movement and balance. Patients with these tumors report problems with hearing and tinnitus more often than they report true vertigo.(8)

Within the brain itself, trauma, growths, interruptions in blood supply, and biochemical imbalances can compromise the processing of sensory information. The result of such a compromise can be a conflict when the vestibular information is compared to the information produced by other sensory systems. These conflicts can result in "neural confusion" and the generation of perceptions, such as vertigo, that do not conform to physical reality (i.e., the patient senses motion when none is occurring). The conflicts can also result in more subtle "psychological" problems including an inability to concentrate, depression, and feelings of fatigue that occur as the brain is forced to devote resources to the problem of straightening out conflicting sensory messages. In fact, the "psychological" problems associated with these information processing conflicts can be so severe that they cause some patients to contemplate self-destructive acts.(42)

Detection of Central Vestibular System Problems
When central problems are caused by tumors or trauma, they are often detectable by using an imaging technique such as computerized tomography (CT scan) or magnetic resonance imaging (MRI).(8) The more subtle information processing problems are harder to detect because the failures are not detectable with conventional imaging techniques. Instead, they must often be inferred from the patient's history, by observation of the patient performing routine tasks, and from the results of more formal neuropsychological testing.

Central Versus Peripherial Vestibular Problems

The nature of the patient's symptoms can help in determining what is causing the problem. For example, data in Table 1 indicate how characteristics of the patient's vertigo can be used to help in determining whether the problem is central or peripheral.(11)

Table 1 Characteristics of Centrally versus Peripherally Caused Vertigo. Reprinted with permission, Dizziness in Primary Care Patients by Warner, EA, et al, Journal of General Internal Medicine, Volume 7, 1992, pages 454-62

Characteristic Central Vertigo Peripheral Vertigo
Duration Long Brief
Intensity Moderate Severe
Nausea/Vomiting Mild Severe
Neurologial Symptoms Common Rare
Hearing Loss Rare Possible
Affected by Head Position Not usually Frequently

Visual System Problems

Just as unreliable or erroneous information from the vestibular system can cause sensory conflicts, unreliable visual information can also create conflicts. Along with dizziness, many patients with visual system problems complain about photophobia, motion sickness, inability to function in situations involving peripheral motion (e.g., moving down the aisle in a grocery store or library), reading difficulties, and anxiety.(43) Common causes of faulty visual information include abnormal eye movements, lack of image clarity, image size differences, binocular conflicts, and field reductions.

Eye Movements
When examining a patient complaining of dizziness, special care should be taken to check for nystagmus or failures of the normal visual/vestibular reflexes. In cases of gross vestibular reflex failure, patients can lose the ability to hold the visual world stable as they move their head and will complain that the world bounces up and down as they walk (oscillopsia).(25,44) Some patients also complain about blur, but, on closer questioning, it will be found that they are really experiencing shimmer or colored fringes on letters possibly because of small nystagmoid eye movements.

Image Clarity
Vision care specialists typically provide lenses that yield the maximum acuity for their patients. Most of the time this approach is successful, but occasionally patients will have trouble adapting to new lenses, especially if the retinal images created are considerably different in size or position as compared to the images produced by the old lenses. This is because the brain has adjusted its expectation to the images produced by the old lenses and the new images create conflicts with the expectation. Another source of conflict might involve conflicts that would occur when the information carried by the new images is compared to the information coming from the vestibular system.

Most patients adjust to their new lenses in a few days or weeks, but some will experience the vertigo, nausea, and discomfort associated with sensory conflict during this adaptation period. A few patients, especially those with vestibular or hyper-vigilance related psychological problems, will be unable to adapt to their new lenses and will be very willing to sacrifice acuity for a reduction in conflict symptoms.

Binocular Image Conflicts
Binocular image conflicts can occur because the images produced on the retinas are of unequal sizes, or because the eyes fail to align properly. Often an image size difference (aniseikonia) is created when lenses of significantly different powers are used to compensate for anisometropia.(45) The resulting difference in retinal image sizes makes it difficult for the brain to fuse the images into a single precept.

Other patients have aniseikonia that occurs without anisometropia; this condition can sometimes be quite difficult to detect. Treatment for aniseikonia can involve the prescription of contact lenses instead of spectacles to reduce the difference in magnification effects, or the use of "size lenses" that can change retinal image sizes.

Ocular alignment problems can involve potential misalignments that require constant effort by the patient to overcome, (e.g., high phorias or fixation disparities), or major problems in which the eyes are significantly misaligned, (e.g., strabismus). These misalignments can be in the horizontal or vertical directions, or they can involve rotation of the eye around the line of sight.

Detection of these problems ranges from simple observation of ocular postures in the case of strabismus, to the need for prolonged occlusion in the case of latent vertical deviations.(43) It is also possible for the misalignment to occur only intermittently (e.g., during periods of high stress), and perhaps only during specific tasks such as reading or when the eyes are in specific positions of gaze.

Patients with normal binocular alignment and those with gross misalignments are often relatively symptom free, whereas those with deviations that are intermittent, small enough to overcome with mental effort, or situation-specific experience the most symptoms. As an adaptive measure, the visual system can develop the ability to suppress a considerable portion of the information from a deviating eye if the deviation is large and constant.(45) However, if the deviation is not large and constant, the brain must work to "sort-out" the information from the two eyes prior to comparing it to the information arriving from the vestibular system. This process can produce symptoms of dizziness in many patients.

Treatment of ocular misalignment involves restoring alignment optically, surgically, or with vision therapy. Care must be taken, however, when attempting to restore binocular vision to patients who have adapted to their deviations by learning to suppress the image from the deviating eye. Often these patients experience an increase in symptoms before they feel better. In some cases, especially with elderly patients, faulty binocular vision can be intentionally disrupted with an occluding filter over one eye to remove a sensory conflict.

Reduction in Visual Fields
The brain uses information from the peripheral visual fields, along with vestibular and other sensory information, to maintain balance and a sense of position in the environment. Restricted fields can, therefore, cause many patients to experience disequilibrium, especially when the field loss is recent.(46) Skills associated with cognitive mapping, the ability to move about in a complex environment, and eye-hand coordination can also be affected by field restrictions.(46)

New Spectacles Can Cause Dizziness

When the head moves from side to side, the vestibular system detects this motion and sends a message to the eye muscle control systems causing the eyes to move counter to the head movement. This allows gaze to be held still as the head moves. The process is called the Vestibulo-Ocular Reflex (VOR). Failure of this mechanism can cause oscillopsia (bouncing vision) when a patient walks or otherwise moves the head.

To operate properly, the ratio (sometimes called the gain) of vestibular movement signals to the amount of compensating eye movements must be correct. If the eyes move too much or too little in response to a head movement, a sensory conflict results and the patient gets sick.

If there is a significant power change in the patient's new glasses, the image has been made larger or smaller on the retina so the VOR gain must be re-calculated by the brain. For some patients this is easy to do (a no-brainer), but for others it takes time - up to several weeks. And some never manage the task. This is why some patients experience transient dizziness caused by their new lenses.

Now consider the patient whose vestibular system is a little shaky to begin with and who needs bifocals or progressive addition lenses. In addition to the distortions on the periphery of the lenses, consider the range of VORs the brain has to calculate. A different one is needed for every spot on the lens because the powers are different at each spot.

CLINICAL PEARL. NEVER GIVE A PATIENT WITH A HISTORY OF DIZZINESS OR VESTIBULAR PROBLEMS A PROGRESSIVE ADDITION LENS. IN FACT DO NOT EVEN GIVE THEM A BIFOCAL. GIVE THEM SEPARATE NEAR AND DISTANCE LENSES SO THAT THE BRAIN HAS TIME TO RECALCULATE THE VOR AS THE PATIENT CHANGES GLASSES.

Vertical Imbalances as Causes of Dizziness

A frequently discussed source of sensory conflict problems is unresolved vertical imbalance. It is often said that vertical imbalances are like hyperopia in that a portion of the imbalance is manifest so that it can easily be detected during a normal examination, and another portion is latent which means that special techniques must be used to reveal it.

One of these techniques is prolonged monocular occlusion which was advocated by Raymond Roy, Sr.(43) Using the Roy technique, patients are monocularly occluded for 3 days per eye. This prolonged occlusion releases the latent vertical which can then be compensated with prism.

Roy developed a sign and symptom list that he believed suggested a latent vertical problem. These include:

- possible vertigo, but not always
- possible autonomic involvement
- chronic sea sickness
- mild nausea
- headache
- vision changes
- "blur", shimmer, jumping
- photophobia, dislike bright lights
- reading problems
- problems with flicker
- difficulty in conversation
- difficulty in crowds
- difficulty in grocery or library
- walk with head down
- driving problems
- problems with bridges, tunnels, multi-lane roads
- reduced ability to remember and to "think"
- lack of sense of closure or completion
- loss of self confidence
- clumsiness
- slurred speech
- poor handwriting
- chronic fatigue
- inability to divide attention
- reduced input channel capacity
- can't handle a lot of sensory or Intellectual information
- poor memory access
- loss of words in conversation
- can't recall names
- anxiety
- depression, possible suicide
- personality changes

Many of these problems are associated WITH sensory conflicts, but others suggest higher level involvement with cognitive processes.

Other problems suggest that peripheral retinal information is somehow causing the patient grief. Classic problems that sensory conflict patients report occur in environments with very busy peripheral information like aisles in grocery stores or libraries. Many patients will not enter these environments without a shopping cart or another person to hold onto for support. Problems with driving over bridges and through tunnels can also be understood as involving lack of a horizon to use for a reference when on top of the bridge or in the tunnel.

 

PSYCHOLOGICAL CAUSES OF DIZZINESS

Dizziness is seen as a presenting complaint in a variety of psychological problems,(42) especially depression and the anxiety neuroses. At one clinic specializing in dizziness, approximately 1 in 5 patients was diagnosed as having a psychogenic etiology for their dizziness, and, at another clinic, the ratio was almost one in three.(4) Although it is easy to dismiss psychogenic dizziness as "all in the patient's head," and thus of little concern, it is quite possible that the initial cause of the psychological problem was physiological (e.g., vertigo caused by a sensory conflict in a high stress situation). For this reason, all dizzy patients should be evaluated for possible physiological problems before making a diagnosis of psychogenic dizziness.

Anxiety Neuroses
About 5% of the population experience significant episodes of unrealistic anxiety (i.e., anxiety that is not appropriate for the situation).(6) This anxiety can be chronic and involve a constant state of heightened internal and external environmental awareness, or it can be acute and occur in the form of panic attacks.(42)

Patients with chronic anxiety often report a constant fear that something bad is going to happen, trembling, frequent sweating, butterflies in the stomach, vague chest pains, palpitations, and other symptoms that suggest the body's flight or fight mechanism is being activated.(23) The dizziness that accompanies these feelings can originate from a variety of sources including vasoconstriction and hyperventilation.

Panic attacks are episodes of acute anxiety that occur for no known reason. They can last from a few seconds to many minutes and are frequently so intense as to be disabling. Sensations include chest pain, near-syncope, dizziness, possible vertigo, intense need to escape from the location where the attack is occurring (i.e., to hide or flee), sweating, and extreme fear.(23) Often patients with panic attacks feel that they are having a heart attack and/or are going to die. These attacks can occur several times per day, or there can be days, weeks, or months between them. This uncertainty intensifies the patient's fear of the attacks, and can result in agoraphobia in which the patient is afraid to leave home. As with chronic anxiety, the dizziness seen during panic attacks probably has a respiratory and/or vascular etiology.(47)

The symptoms associated with chronic or acute anxiety are the same as those seen in conditions having more readily defined "physiological" causes (e.g., sensory conflict), and it has even been suggested that some anxiety episodes are caused by a heightened responsiveness to the sensations produced by sensory conflicts. In addition, many conditions, such as vestibular or visual disturbances, have anxiety as a symptom, so great care must be exercised when a diagnosis of dizziness caused by an anxiety neurosis is made just because no other explanation could be found.(42)

Hyperventilation Syndrome
To function properly, the body maintains relatively tight control over its internal environment. Temperature, pH, osmolarity, oxygen/carbon dioxide balance and other factors are typically well regulated through the use of various receptors and feedback loops. In the case of oxygen/carbon dioxide balance, however, this regulation can be upset when the patient's pattern of breathing is altered and hyperventilation occurs.(47) Symptoms can include air hunger, difficulty breathing, numbness or tingling around the mouth and in the extremities, dizziness, and possibly near syncope or syncope. Treatment ranges from breathing into a paper bag to restore the body's oxygen/carbon dioxide balance,(25) to the use of medications to suppress the anxiety that can trigger the hyperventilation. If actual syncope occurs, the body typically restores the proper balance without further intervention.

It is often impossible to determine whether hyperventilation creates anxiety, anxiety creates hyperventilation, or possibly a third factor such as sensory conflict creates both conditions. By the time the patient is seen, even if a treatable sensory conflict originally caused the problem, the anxiety (and dizziness) could have taken on a life of its own and can persist after the sensory conflict has been resolved.(42)

REDUCTION OF BLOOD FLOW TO THE BRAIN

Along with a proper chemical balance, the brain must also have an adequate supply of blood to function properly. Maintenance of the blood supply requires the heart to pump blood in proper quantities and at the proper pressure through patent blood vessels. Compromising either the heart or the vessels can result in a variety of problems, one of which is often dizziness. Occasionally it has been suggested that hypertension itself can be a direct cause of dizziness, but it is more likely that one of the indirect consequences of hypertension such as cardiac or vascular abnormalities actually cause the dizziness.(6)

Cardiac Problems
Because the heart is a mechanical device with pump chambers, valves, and an electrical control system, failure of any component can result in reduced blood flow to the brain. Some failures, such as myocardial infarctions, are catastrophic, but others, such as arrhythmias, valves that do not close completely, or muscle weakness can result in either chronic or episodic reduction in blood flow. When these problems occur, the patient might be aware of chest sensations (e.g., in the case of some arrhythmias), or they might experience dizziness related to near-syncope or syncope.(5,7,11) If the cardiac problem is chronic, it can often be detected by the use of traditional electrocardiography, or echo-electrocardiography.(48) If the problem is episodic, accurate diagnosis could require the patient to wear a portable cardiac rhythm recorder (e.g., Holter monitor) until an episode occurs.(11) Some episodic problems occur as a result of excessive vagal activity that produces transient bradycardia (i.e., slow heart rate). This excess vagal activity can result from anxiety and lead to dizziness, near-syncope, or syncope.(11) Patients can occasionally aid in the diagnosis of cardiac rhythm disturbances by monitoring the pulse rate and regularity during episodes of dizziness.

Vascular Problems
Vascular problems limiting blood flow to the brain can also be chronic or acute. Chronic problems usually involve deposits that have built up on the walls of the vessels (e.g., atherosclerosis). Acute problems can involve mechanical obstructions such as clots or plaques that have become lodged at narrow spots in the vessels.(49) Other acute problems can be neural in origin such as excessive vagal activity that can cause constriction of the vessels supplying blood to the brain.

PHARMACOLOGIC CAUSES OF DIZZINESS

CLINICAL PEARL. BEFORE YOU START A COMPLEX DIAGNOSTIC SERIES TO EVALUATE A PATIENT'S DIZZINESS, ASK WHAT DRUGS THEY ARE TAKING. YOU WILL FIND THAT DRUGS ARE CAUSING THE PROBLEM IN A VERY HIGH PERCENTAGE OF PATIENTS.

Perhaps the most important question that should be asked after a patient has described a problem with dizziness is: "What medications are you taking?" A brief review of any standard reference on pharmacology will show that drugs ranging from aspirin to cold medications (and even to the drugs actually used to suppress dizziness) have dizziness as a possible side-effect.

A search through the computer accessible version of the Physician's Desk Reference revealed that of the more than 4000 drugs listed, over 25% had dizziness listed as a possible side-effect.(50) This should not be too surprising when the various etiologies of dizziness are considered. For example, medications such as the diuretics change the body's osmolarity and this can affect the inner ear. Hydrochlorothiazides and alpha1 blockers such as prazosin can cause dizziness as can calcium channel blockers such as verapamil.(27) These effects can be potentiated when multiple drugs are taken.

Long-term or high-dosage use of some medications such as the aminoglycosides can actually damage the inner ear.(8) In the case of streptomycin, the damage involves the vestibular hair cells beginning in the crista of the semicircular canals and extending to the otoconia in the utricle and saccule.(29,51)

Other medications that reduce blood pressure can create postural hypotension and dizziness (e.g., beta blockers). Still others create anxiety which results in dizziness (e.g., some decongestants and diet pills). Sometimes, sorting out the dizziness caused by the patient's disease from the dizziness caused by the medications used to treat the disease can be very frustrating.

SPECIFIC DISEASES AND AGE RELATED FACTORS ASSOCIATED WITH DIZZINESS

Many systemic and focal diseases can produce sensations of dizziness

Specific Diseases
Dizziness is a common problem accompanying relatively benign diseases such as colds and influenza. In these cases, the dizziness can result from occlusion of the eustachian tubes, inflammation of the middle or inner ear, dehydration and resulting osmolarity changes, elevated temperature, or even the medications taken for symptom relief.

Other diseases producing dizziness are more significant. Perhaps the most common neurological disease is multiple sclerosis in which the myelin sheaths of the nerves are affected.(13) In this disease, one of the early targets can be the optic nerves. The resulting optic neuritis distorts the information sent to the brain and this can result in sensory conflict. Similar problems can affect the eighth nerve and the parts of the brain responsible for balance and muscular control; it is common for patients with multiple sclerosis to report disequilibrium and dizziness.

Age-related Problems
The syndrome of multiple sensory deficits is probably the most common cause of disequilibrium in the elderly.(4) The syndrome can be caused by a combination of visual impairment, vestibular anomalies, peripheral neuropathies, or orthopedic problems, including cervical spondylosis, osteoarthritis and muscle weakness.(11) Parkinsonism, cerebellar disease and frontal lobe apraxia are other important causes of disequilibrium.(11)

Aging can also make patients more susceptible to the adverse reactions of medications. Antianxiety agents, such as the benzodiazepines (e.g., diazepam, chlordiazepoxide, and lorazepam) have been reported to cause dizziness, and this side-effect is especially prevalent in the elderly.(51) It is also common for the elderly to be taking diuretics that can affect the inner ear, or hypertension medications that can make them susceptible to orthostatic hypotension.

MANAGEMENT OF DIZZINESS

Dizziness is typically a symptom of an underlying problem, so management requires accurate diagnosis and appropriate treatment of the underlying problem. The various signs and symptoms that are grouped together and called dizziness are just that - signs and symptoms. As such, management would ideally be directed toward correction of the underlying problem. Unfortunately, this can be easier said than done.

Sometimes the causes are multiple and interacting. For example, if a patient with a marginal visual system and a marginal vestibular system, is given a drug that alone would not cause a problem, the result can be dizziness. Or an elderly patient with poor vestibular function could develop cataracts that reduce her ability to use vision for balance.

Often, time is required playing detective in areas that are not associated with eye disease. Too frequently dizzy patients have seen their "eye" doctor and been told that they do not have glaucoma - so go bother someone else. Or they were told that their problems are all in their heads, so take tranquilizers or quit your high-stress jobs. This frustrates patients who know that something really is going wrong in their heads, so they go from doctor to doctor becoming "thick file" patients.

Few "disease" doctors want to take the time and experience the frustration associated with managing dizzy patients. This is especially true if your managed care plan allocates you 12 minutes per patient. What to do? It can be argued that you owe dizzy patients a complete visual evaluation to detect cases of ocular imbalance that might contribute to the problem. You also owe these patients an attempt to make a differential diagnosis, and, if you cannot manage the problem yourself, you owe them an intelligent referral - not just a bounce back to their GP.

Visual/Vestibular Conflict Therapy
If a sensory conflict is suspected, thorough examinations of the visual and vestibular systems are required. If ophthalmic problems are found, they can usually be corrected by the use of lenses or vision therapy. In the case of vestibular problems, the treatment might require surgery to close a perilymphatic fistula (52) or remove a tumor, antibiotics to treat an infection, dietary restrictions to maintain a constant state of blood osmolarity, or the use of diuretics. In extreme cases, surgical or medical destruction of the vestibular apparatus or the vestibular portion of the eighth nerve might be required to provide relief for the patient.(53)

In other cases, simple procedures have been shown to dramatically reduce dizziness. For example, it has been suggested that BPPV is caused by dislodging the tiny calcium deposits that are normally attached to the hair cells in the inner ear. To treat this condition, the patient lies supine on a table with his or her head hanging off the side. The clinician then rotates the patient's head to the side until the dislocated calcium deposits move away from the part of the inner ear where they are causing problems.(8,53A) The patient then maintains an upright posture for 48 hours to allow the calcium deposits to settle into a less troublesome location. Using this treatment, Baloh has reported to have achieved a 90% first treatment cure rate.(54)

Habituation Exercises
If the problem causing the dizziness cannot be found or treated, sometimes it is possible to reduce the patient's awareness of the dizziness by habituation to the situation or stimuli that cause dizziness. This habituation is similar to what ice skaters and acrobats goes through as they learn not become dizzy as a result of spinning.(54)

Dynamic Adaptive Vision Therapy developed by Gillilan to treat motion sickness is an example of habituation training.(55) The therapy involves the use of various devices including a lettered ball suspended from the ceiling. In some exercises, the patient is asked to watch the ball as it moves, or shift gaze between various objects until symptoms are produced. The patient is then allowed to relax until the symptoms dissipate. This is followed by exposure to the provocative stimuli again. Gradually, over a four to eight week period, the patient's tolerance for the stimuli increases as habituation or adaptation occurs. In successful cases, the symptoms totally disappear by the end of therapy and the patient remains symptom free for years.(55)

Physical Therapy
Many patients with vertigo or disequilibrium have trouble standing or walking; in these cases, physical therapy might be very helpful.(55a, 55b) Specific exercises can be designed to help the patient adjust to balance difficulties, learn new methods of coping with the problems, or even attempt to reduce the level of the problem by use of habituation exercises.(30,56)

A commercial posturography test unit known as the Equitest can be used diagnostically and to monitor the dizzy patient's progress.(57) The patient stands on a platform and receives stimuli that produce potentially deceptive outputs from one of the body's sensory systems (e.g., visual or proprioceptive). The visual and/or proprioceptive information can be altered, or vision can be occluded; then the platform is moved and the patient's response is analyzed. Posturography can be used to identify which sensory system(s) are responsible for the patient's dizziness/balance problem and to evaluate rehabilitation procedures.(39,57,58)

Psychotherapy
Most subjects experiencing dizziness will also experience concomitant anxiety, especially until a physiological cause for the dizziness is found. If the underlying disorder can be treated promptly, the anxiety is usually of little consequence. However, if no physiological cause is found, or if the underlying cause is not treatable, psychotherapy can help the patient adjust to the disability produced by the dizziness. Psychotherapy can often prevent the anxiety from developing into a major psychological problem such as agoraphobia.

Anxiety reduction techniques such as diaphragmatic breathing can also be taught during psychotherapy. This is especially valuable in cases involving dizziness associated with hyperventilation.(4)

Medical or Surgical Enhancement of Blood Flow
If the patient suffers from episodes of near-syncope or syncope, evaluation of the cardiovascular system might indicate the need for medication or surgery to enhance blood flow. For example, a malfunctioning heart valve may need repair or an endarteriectomy might be necessary to restore blood flow blocked by atheromatous plaques.(48)

Medications Used to Suppress Symptoms
If the cause of the patient's dizziness cannot be found or treated, medications might be used to suppress the symptoms.(30) These medications fall into several categories: antihistamines, anticholinergics, diuretics, and anti-anxiety agents.

Antihistamines
Antihistamines are the mainstay of both over the counter and prescription anti-dizziness medications. Although there is still some question regarding their mode of action, the most commonly accepted theory is that they work by suppressing the output from the vestibular system.(27)

Common drugs used to manage dizziness are listed in Table 2.(27,59,60) Although these drugs are mainly antihistamines, they also have anticholinergic properties so they can cause drowsiness (and possibly anxiety reduction) as adverse reactions.

Table 2 Antihistamines Effective for Suppression of Dizziness(25,27,60)(b)

Generic Names Brand Name Dosage
Dimenhydrinate Dramamine® 50 mg TID
Diphenhydramine Benadryl® 25-50 mg TID
Meclizine Antivert® 25-50 mg BID
Promethazine Phenergan® 25 mg QD

Anticholinergic Agents
Scopolamine (Transderm Scop®) is the only medication in this category commonly used in the management of dizziness; it is also effective against the nausea and vomiting associated with motion sickness.(16,27,30) The delivery vehicle is a skin patch placed behind the ear a few hours prior to the offending activity. One patch will release scopolamine for 3 days. (For a time the patch was removed from the market but might now be available again.)

Scopolamine's mechanism of action is not completely understood, but it might act within the central nervous system(60) and/or on the vestibular system itself. Scopolamine is a potent anticholinergic with significant adverse reactions; they include drowsiness, dry mouth, mydriasis, and accommodative dysfunction.(27)

Antidepressant/Antianxiety Agents
Dizziness can produce anxiety and depression, but anxiety and depression can also produce dizziness. This circular relationship suggests that most patients experiencing dizziness would benefit from the use of an antianxiety or antidepressant medication. If the underlying disorder is psychogenic in nature, this is probably true. But, if the dizziness is caused by sensory conflict or disequilibrium, these medications can sometimes exacerbate the problem. This is because the tranquilizing effects of these medications make it harder for the brain to resolve conflicting sensory messages and keep the body balanced. Nevertheless, antianxiety agents are frequently prescribed because the symptoms of dizziness are so upsetting to the patient.

Antianxiety agents can help patients to cope with their dizziness and some agents (e.g., Xanax®(61)) can block panic attacks and the resultant near-syncope and hyperventilation. These drugs appear to act peripherally by relaxing large muscles, and/or centrally on the limbic system, thalamus, and/or hypothalamus to produce their effects.(27,60)

For reasons that are not yet clearly understood, several antidepressant agents can lessen the severity of ill-defined lightheadedness found in some mood disorders. The main drugs in this category are the tricyclics, heterocyclics, monoamine oxidase inhibitors, and phenothiazines.(25,59) All appear to exert their effects on the monoamine neurotransmitter/receptor system.(60)

Some of the commonly prescribed antidepressant and antianxiety agents that might be used in the management of dizziness are listed in Table 3.

Table 3 Commonly Prescribed Anti-Depressant and Anti-Anxiety Agents(25,27,60)(b)

Generic Name Brand Name Indication Dosage
Amitriptyline Elavil® Depression 25 mg TID
Fluoxetine Prozac® Depression 20 mg QD
Phenelzine Nardil® Depression 15 mg TID
Thioridazine Mellaril® Depression 25 mg TID
Diazepam Valium® Anxiety 2 mg TID
Alprazolam Xanax® Anxiety 0.25 mg TID
Buspirone Buspar® Anxiety 5 mg TID


Diuretic Medications
These agents have shown some promise in treating Ménières syndrome and endolymphatic hydrops. They appear to function by correcting or stabilizing the osmotic balance in the inner ear fluids. The most commonly used diuretics are the thiazides and their combination formulations.(8,25,59)

Acetalazolamide (Diamox®) has also been used for this purpose.

Calcium Antagonists such as flunarizine, seem to have a vestibular sedative effect and might have applications for the suppression of dizziness related to vestibular malfunction.(62,63)

Betahistine is a new drug for the suppression of dizziness associated with vestibular disorders, especially Ménières disease.(62,64-66) The exact mechanism of action is unknown, but it is possible that betahistine acts as a vasodilator to increase cerebral blood flow, and/or that it has direct effects on vestibular neurons.(66)

SUMMARY

Although dizziness is a relatively common patient complaint, it is often difficult to understand exactly what sensations the patient is experiencing. Careful history taking will help to define the sensations more fully and classify them as vertigo, near-syncope, disequilibrium, or ill-defined lightheadedness. The correct classification is important because this can suggest a diagnosis and management plan.

Some types of dizziness are relatively easy to manage (e.g., problems caused by improper spectacle lens powers), but most involve the failure of a peripheral sensory system or the failure of the brain to process information correctly. In either case, diagnosis and management often requires a team approach including one or more specialists (e.g., optometrists, neuro-otologists, neurologists, etc.). If the problem causing the dizziness cannot be eliminated, physical therapists and/or psychologists can help the patient adapt to the resulting disability.

Dizziness is a very uncomfortable and disconcerting problem for many patients,(67) especially when its cause cannot be found. It can cause a significant decrease in the patient's quality of life, therefore complaints of dizziness must be taken seriously. Dizzy patients can experience profound depression associated with their dizziness and professionals who work with these patients should be alert for warning signs of self-destructive behavior.

Acknowledgments

Some of the material in the vestibular section of this paper has been drawn from information provided by the Vestibular Disorders Association (VEDA). Patients with vestibular problems or health care providers who want more information on this topic can contact VEDA at PO Box 4467, Portland OR 97208-4467; (503) 229-7705.

The project was completed while Major Anderson was enrolled in the Clinical Optometric Management Masters program at the Pacific University College of Optometry. The views expressed in this article are those of the authors and do not necessarily reflect the positions of the Department of the Army or the Department of Defense. The U.S. Government is authorized to reproduce and distribute reprints of this article for governmental purposes not withstanding any copyright notice hereon.

Footnotes

a. An earlier version of this article appeared as THE DIZZY PATIENT: A REVIEW OF ETIOLOGY, DIFFERENTIAL DIAGNOSIS, AND MANAGEMENT, by Douglas C. Anderson, OD, Robert L. Yolton, OD, PhD, A. Richard Reinke, OD, Paul Kohl, OD, and Laurie Lundy-Ekman, PhD, PT in the Journal of the American Optometric Association; 1995 66(9):545-58 copyrighted by the American Optometric Association. This modification of the original paper is by permission of the American Optometric Association.

b. Drug schedules and dosages are believed to be accurate at the time of writing but must be confirmed prior to actual implementation.

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Address correspondence regarding the content of this article to:
Robert L. Yolton, PhD, OD
Pacific University College of Optometry
2043 College Way
Forest Grove OR 97116
yoltonr@pacificu.edu
Note:
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