Chapter 14 - Evaluation of the “dizzy” patient
Dizziness is a common symptom in neurologic practice as well as primary care. According to the National Ambulatory Medical Care Survey, about 7% of primary care visits by patients aged 85 or above are for dizziness. This makes the symptom of dizziness, one of the most common in general practice. Neraly 20% of elderly patients reported having dizziness within the past year that either restricted their activity or require them to see a physician. Therefore, it's necessary to have an understanding of dizziness and a systematic approach to evaluating these patients. Most of the causes are benign (notwithstanding significant impact on activities and quality of life). There are a few serious causes and these must also be considered in diagnosis. Unfortunately, there is no simple and reliable method to identify those patients with serious underlying causes further increasing the need for a systematic approach to evaluation.
The main goal of the history is to determine exactly what the patient means by the term “dizziness”. There are generally four things that patients mean by “dizziness” and each requires a distinct process of evaluation. These four types include vertigo, presyncopal lightheadedness, disequilibrium and other (usually described as a floating type of sensation). Since these terms are usually not familiar to patients, it is necessary for you to determine what the patient means during the history.
Vertigo is defined as the illusion of movement. Questions such as "does it feel like you're on an amusement ride," and "are you sick to your stomach with the dizziness," suggest that they have vertigo. Usually patients who are experiencing vertigo at the time of evaluation can tell you the specific direction of the motion.
Pre-syncope is a feeling of faintness or lightheadedness. Questions such as "do you feel like you might pass out," or "does it feel similar to when you stand up too fast," are questions which suggest that the patient is describing pre-syncope.
Disequilibrium is the feeling of being unsteady on one's feet. Typically, this improves quite a bit when there are other sensory cues (such as the ability to touch things) and is much worse. when the patient's vision is blocked, or when the surface on which they are walking is very uneven. Questions such as "does it only happen when you're on your feet" and "does it get much better if you touch things" are very useful. Additionally, disequilibrium is probable if the patient notes that the sensation is substantially worse in the dark or when they are in the shower.
Older patients may well have more than one kind of dizziness. Therefore the question of "how many kinds of dizziness, do you have," is often a useful question, since each require separate evaluation.
Once you have defined what the patient means by dizziness, it is important to understand the timing of the dizziness, whether it appears constantly or in attacks, what they do when they experience dizziness and whether there are any associated symptoms (such as hearing change, nausea, etc). Also, when there are attacks, the duration of the attacks as well as whether there are any things that provoke them (such as movement, loud noise or pressure changes) are important clues to cause.
We will discuss the diagnostic evaluation of each of the major categories of dizziness.
Vertigo, the illusion of movement, is due to imbalances of signals to the vestibular apparatus. This can either be due to peripheral or central causes. Peripheral causes relate to damage of the inner ear receptors or to the vestibulocochlear nerve. Central causes include damage to centers that process vestibular signals in the central nervous system. Most of these centers are located in the brain stem, including the vestibular nuclei and the vestibulocerebellum. There are also portions of the cerebral cortex that process vestibular signals, although these are less common causes of vertigo. Signs and symptoms can usually distinguish peripheral from central causes of vertigo.
Peripheral vertigo. Peripheral vertigo results from damage to the inner ear or the vestibulocochlear nerve. Since one of the main roles of the vestibular system is to stabilize the eyes during head movements, abnormal vestibular function usually produces abnormal eye movements. Specifically, it is associated with jerk nystagmus (to and fro movements of the eyes with a slow and fast component; see Chapter 6). With peripheral causes of vertigo, the nystagmus is in one particular direction (named by the fast phase of the jerky movement). Nystagmus will always worsen when the person moves their eyes toward the direction of the fast phase. In peripheral vertigo, nystagmus is either horizontal or rotary. There may be hearing loss or tinnitus due to accompanying damage of the auditory mechanism. There should be no other signs of damage to the nervous system, although the patient may be unable to walk if the vertigo is severe enough (they tend to veer one way). Peripheral vertigo should not be accompanied by any other sign of damage to the nervous system (such as: incoordination of the hands; diplopia or dysconjugate eye movements; loss of sensation; or weakness). The patient is likely to experience nausea or "motion sickness," But should not have other systemic signs. Typically, you can predict how vertiginous the patient is by how rapid the nystagmus is. This is because both are being driven by the imbalanced signals from the two inner ears (see Chapter 6).
Central vertigo. Central vertigo is typically milder than peripheral. The amount of nystagmus is usually greater than the patient’s illusion of movement. Additionally, the nystagmus may be in multiple directions or possibly in a vertical direction (upbeat or downbeat). Central vertigo is not associated with hearing loss, and there are often other abnormalities of the central nervous system found by examination.
The causes of central vertigo and peripheral vertigo are quite different. Peripheral vertigo is much more common.
The most common causes of peripheral vertigo are benign. These include benign paroxysmal positional vertigo (BPPV or often just BPV), cervicogenic vertigo, acute labyrinthitis/vestibular neuronitis, Meniere syndrome and perilymph fistula.
The most important questions that you should ask the patient with peripheral vertigo include: whether it occurs in attacks; whether there is anything that sets it off; whether there are symptoms accompanying it; and whether there has been any drug or toxin exposures. The most common things precipitating attacks of vertigo include movement, loud noises, changes in pressure (such as airplanes, Valsalva maneuver, coughing, sneezing) or trauma. Keep in mind that all causes of vertigo feel somewhat worse when the patient is moving.
Peripheral causes of vertigo tend to produce repeated attacks and these tend to be recognized by the circumstances that provoke the vertigo. A relatively common and isolated condition is “vestibular neuronitis” or “acute labyrinthitis.” This condition is believed to be inflammatory, though the precise etiology is not known. It results in a single, monophasic attack of vertigo. The attack may follow a viral syndrome or be completely "out of the blue". Symptoms typically come on quickly and resolve over days up to a few weeks. In more severe cases, it may be many weeks before the patient feels completely well.
Another condition that should be considered in the evaluation of the patient with vertigo is acoustic neuroma. This typically produces mild vertigo (if any) because it is so slowly growing. It is much more commonly found in the investigation of hearing loss. Nonetheless, this benign tumor is a consideration in the patient without other clear cause of vertigo.
Most other causes of vertigo appear in attacks or with clear precipitation. We will discuss these causes in the following sections.
Benign positional vertigo. If movement precipitates attacks of vertigo considered BPV, vertebrobasilar artery insufficiency or cervicogenic causes. Of these, BPV is by far the most common. This may develop spontaneously in the elderly, or may be provoked by head trauma. The head positions that classically bring on attacks include looking up (such as when trying to reach a high shelf), bending over to tie one’s shoes and rolling over in bed. Several seconds after the head movement, the vertigo begins quite suddenly. The vertigo reaches a maximum within seconds of onset and gradually improves over 15 to 60 seconds, sometimes leaving the patient feeling queasy, but otherwise unharmed. The Hall Pike, or Nylan-Barany maneuver (see Figure 6-10) can often reproduce the symptoms. Treatment with the cannilith repositioning maneuver is often effective. Because this probably is due to loose otoliths in the inner ear, and since these are composed of calcium carbonate crystals, they may dissolve on their own over a period of weeks to months. This will terminate the tendency to have these attacks. However, they can return as more otoliths become liberated at some future date.
Cervicogenic vertigo. Cervicogenic vertigo is typically provoked by movement or sustained postions of the neck. There is usually upper neck pain and often restriction of motion in the area. Usually, the symptom of vertigo begins quickly when the neck is moved and remains during the period of sustained head position. The amount of vertigo (and any nystagmus) is typically much less than with BPV. This is not common, although it can be seen after head and neck injuries.
Vertebrobasilar insufficiency. The vertebrobasilar artery may be compromised by neck rotation. If this is the cause of positional vertigo, symptoms should gradually build after a lag of five to 15 seconds necessary to produce ischemia. This is also uncommon, but requires investigation of the posterior circulation when it does occur.
Precipitation of attacks of vertigo by loud noises suggests Meniere syndrome or perilymph fistula. Meniere syndrome is associated with increased pressure in the endolymph of the inner ear. The high pressure is believed to result from diminished resorption of the fluid. With the high pressure, there may be small ruptures in the membranes containing the endolymph, causing sudden mixing of the endolymph and perilymph ( which are fluids of very different composition). This produces a sudden change in pressure and in electrical charge across the membranes of the inner ear. Attacks can last 30 minutes to several hours, until equilibrium is reestablished. Over months to years of attacks, there is cumulative damage to vestibular and cochlear hair cells. This results in decreased auditory acuity to low tones and a low-pitched tinnitus (often a humming or buzzing). Perilymph fistula, results from a small leak between the inner ear and the air-filled middle ear. This leak may be provoked by a minute disruption in the wall of the inner ear or round window due to trauma (or barotrauma). This permits escape of perilymph particularly at times of high inner ear pressure. The sudden change in inner ear pressure due to leakage of this fluid may trigger episodes of vertigo as well as producing some chronic damage to hair cells. Changing pressure in the external ear (such as with insufflation through an otoscope) may also precipitate attacks in both of these conditions. This has been termed "Hennebert's sign." Although this has also been suggested as a “fistula test”, this is not specific for perilymph fistula. Precipitation of attacks by changes in pressure (airplanes, driving in mountains, Valsalva) is more characteristic of perilymph fistula. However, this is also not completely definitive.
Head and neck trauma may precipitate vertigo in several ways. It may result in a perilymph fistula, or loosen otoliths (contributing to BPV). Whiplash injury to the neck can produce cervicogenic vertigo and head trauma can result in direct concussion of the inner ear hair cells. In the case of "labyrinthine concussion", gradual improvement is expected.
Vertebral artery dissection is a rare but serious condition that can result from neck injury. This may occlude branches that go to the vestibular area of the brain stem or cerebellum and produce vertigo due to stroke.
Finally, there are studies suggesting instability of the regulation of intracranial blood flow after head and neck injuries. This can produce vertigo or, more commonly, presyncope as part of a "postconcussion syndrome".
The association of hearing loss with vertigo points to inner ear or nerve pathology. In such cases, Meniere syndrome, perilymph fistula or acoustic neuroma should be high on the list of considerations.
Many drugs and medicines can cause dizziness. Those that cause actual vertigo typically have a direct effect on hair cells of the inner ear and it is valuable to review the medications of patients with vertigo.
The Central causes of vertigo, include cerebrovascular disease (including transient ischemic attacks), multiple sclerosis, Chiari malformation and any other conditions directly damaging the caudal brain stem or the vestibulocerebellum.
Chiari malformation represents a particularly challenging diagnosis. This condition is defined by protrusion of the lower portion of the cerebellum through the foramen magnum. This compresses the caudal brain stem and vestibular areas. It is often associated with an occipital headache, and downbeat nystagmus, which strongly suggests an abnormality at the craniocervical junction.
Migraine represents a rare, but difficult to diagnose cause of vertigo. The vertigo is usually a part of the aura of migraine and when the patient has a clear history of migraine following it, the diagnosis may be clear. However, many patients can have migraine aura, without a characteristic headache. In such cases, diagnosis may be difficult.
Laypeople often use the term “dizziness” to describe the sensation of lightheadedness or an impending faint. This symptom results from diffuse cerebral ischemia, and it typically arises from vascular, autonomic or cardiac causes. The most serious of these causes include those related to cardiac disease, such as arrhythmia, outflow obstruction or low cardiac output states. Fortunately, these are rare, but may be difficult to rule out. It may be important to monitor cardiac rhythms during an attack via a Holter monitor or an event Monitor (if episodes are infrequent). An echocardiogram can stratify risk for outflow obstruction or low cardiac output states.
Autonomic failure typically results in postural or orthostatic hypotension. This may occur as part of neurologic conditions such as certain types of polyneuropathy (particularly diabetic neuropathy) or certain disorders of the CNS (such as Parkinson disease). Many medications can also exacerbate or bring on postural hypotension at times.
Vasovagal or vasodepressor episodes are common and may show inappropriately slow heart rates around the time of the attacks, along with low blood pressure. However, between attacks, it may only be possible to identify such patients by sophisticated tests (such as tilt-table tests) or by the setting in which they occurred. These episodes are most commonly brought on by high stress or anxiety. Additionally, anxiety states with hyperventilation can cause presyncope and can also be challenging to diagnose unless the clinical setting is recognized. Hyperventilation results in cerebral vasoconstriction due to the loss of carbon dioxide and the attendant change in blood pH. Hyperventilation is a physiologic response to stress and patients are typically unaware that they are hyperventilating. Hyperventilation may be diagnosed by having the patient overventilate for three minutes while they are in the supine position. The object is to see if this precisely reproduces their symptoms. Finally, migraine can also produce presyncope (probably due to some cerebrovascular instability). This can also be challenging to diagnose unless the proper clinical setting is recognized.
This is a common type of dizziness in the elderly. This is due to disturbance of sensory or motor control systems that are necessary to maintain the upright posture. The most common cause, by far, is multisensory deficit. This typically occurs with gradual decrease in sensory acuity in several systems. Usually there is diminished sensitivity to joint position in the feet, along with some decreased sensitivity of the inner ear balance organ. The symptoms typically are exacerbated in situations where the vision is obstructed (or if the patient has other conditions decreasing visual acuity). This kind of deficit usually shows dramatic improvement when the patient touches or holds onto a stationary object (replacing the loss sensitivity feet with the sensitivity of the hands). Many of these patients have a condition such a polyneuropathy that is damaging peripheral nerves, although many elderly patients lose some sensation in the feet without specific cause. Typically, these patients improve with a cane or other gait assistive device.
Patients with Parkinson's disease or cerebellar disease often have disequilibrium due to motor difficulties. This limits their ability to respond to the changing conditions of ambulation. Slowed responses in Parkinson's disease or incoordination and cerebellar disease may make the patient entirely unable to walk safely. The patient perceives this as disequilibrium. Therefore, the evaluation of the patient with disequilibrium requires both testing of sensation and testing of motor function, including strength, tone and coordination. The vast majority of cases of disequilibrium are due to sensory difficulties, however, and these improve dramatically when patient touches a stationary object.
Vague and difficult to describe dizziness is a common feature of anxiety or psychological distress. This is often described as floating and occasionally as lightheaded. Sometimes evaluation can reveal evidence of hyperventilation, but this is largely a clinical diagnosis.
In summary, dizziness is common. There are three basic types of dizziness, vertigo, pre-syncope and disequilibrium. Each of these types of dizziness requires individual assessment, and many elderly patients have more than one type.
Define the following terms:
vertigo; presyncope; disequilibrium; jerk nystagmus; Meniere syndrome; benign paroxysmal postional vertigo; canilith repositioning (Epley) maneuver; perilymph fistula; Hennebert sign; fistula test; Chiari malformation; acoustic neuroma; tinnitus.
14-1. What types of dizziness are there?
14-2. What questions would lead you to suspect that the patients "dizziness" is vertigo? presyncope? disequilibrium?
14-3. What are the possible causes of vertigo?
14-4. How can you distinguish peripheral vertigo from that caused by damage to the central nervous system?
14-5. What conditions can cause vertigo provoked by movement?
14-6. What conditions can cause vertigo provoked by loud noise or by pressure changes?
14-7. What conditions that are associated with vertigo can be provoked by head or neck trauma?
14-8. What conditions that are associated with vertigo also usually produce hearing loss?
14-9. What are some central causes of vertigo?
14-10. What are some potential causes of presyncope?
14-11. What are some potential causes of disequilibrium?