Dizziness and Vertigo Flashcards
Nearly 20% of elderly patients experience dizziness every year that restricts their activity. Before we discuss what the patient means by dizziness, think for a moment what it means to you? List some of the symptoms that might cause a patient to complain of “dizziness”.
“Dizziness” is a vague term that means different things to different people. It is used most often to describe faintness, loss of balance when walking and vertigo, but it is also used to describe double-vision, dissociation from the world due to depression, drug intoxication and giddiness.
How do we do this! Let’s start with faintness, the feeling that we are going to black out. Most of us have experienced this feeling when we stood up very quickly from a prolonged squatting position. How many different conditions can you think of that produce faintness?
Quickly getting up from a squatting position can cause a sudden drop in blood pressure, reduce cerebral perfusion and result in a blackout or faint. Any condition that reduces intravascular volume can produce orthostatic hypotension and postural faintness. This includes bleeding, prolonged vomiting, severe diarrhea, polyuria and dehydration.
If the heart cannot speed up to compensate and increase cardiac output, then cerebral perfusion fails even earlier. That might occur if a patient were taking a beta blocker and could not easily increase the heart rate on becoming moderately dehydrated. Other medications may reduce blood pressure either as a therapeutic or as a side effect.
What other things common cause faintness?
Patients with diabetes, amyloidosis, Guillain Barré syndrome and certain other disorders can develop an autonomic neuropathy so that peripheral vasoconstriction mediated by the sympathetic nervous system fails to respond to orthostatic falls in blood pressure.
Finally there is the common faint, also called a vasovagal reaction, which can be induced by a variety of stimuli such as viewing your first autopsy.
Syncope can occur when cardiac output falls. In the presence of a beta blocker the heart may fail to accelerate in response to reduced venous return when arising from a squatting position. Can you think of any other cardiac disorders that can cause syncope?
Cardiac causes of syncope and near-syncope include:
cardiac arrhythmias,
heart failure,
obstruction of cardiac outflow (aortic valvular stenosis, cardiac tamponade) and
pulmonary embolism.
Get a cardiology consult
Another huge problem for doctors and for society is the propensity for the elderly to lose their balance and fall. This causes a variety of broken bones, such as hip fractures, and can be followed by a variety of medical complications and constitute the final and last admission to a hospital. Why do the elderly fall so much?
More often than not, the reasons are multifactorial.
Cerebellar dysfunction due midline (vermian) disease from alcoholism or stroke can cause a wide-based ataxic gait.
Vestibular dysfunction from prior trauma or infection may cause the patient to react less quickly to changes in body position when turning.
Vision typically fails due to macular degeneration and cataracts so that it becomes far easier to stumble in dim lit rooms. Loss of position sense in the legs can be compensated with visual input but not if you can’t see well or are in a dark room and so uneven surfaces become especially hard to navigate.
Even without a specific disease process, all of these and other networks are undergoing neuronal depletion with aging. The redundancy in neuronal circuits is lost and a simple task such as gait must be accomplished with marginally functional neural reserves.
Other networks affected by aging or disease include:
the spinal cortical pathways and other associated motor pathways such as rubrospinal, reticulospinal and vestibulospinal pathways.
Disease of the basal ganglia can cause Parkinsonism and produce gait abnormalities such as ignition failure, freezing, shuffling and turning en-block.
Non-neurological problems are very common and include arthritic pain of the hips and knees.
All of this cause the elderly to limit their walking and that produces disuse muscle atrophy, further weakness and worsens osteoporosis.
They become a walking or non-walking time bomb for a fall. Then throw in drug toxicity or dehydration on top of everything, and it is not at all surprising why falls in the elderly present such a huge problem.
One common attribute in the elderly, especially in those with longstanding hypertension, is what?
small vessel disease affecting the white matter of the brain, and for unclear reasons, the frontal areas are affected the most. T
his disconnects the frontal lobes responsible for planning gait from the basal ganglia that permit the smooth coordination of gait, and patients can develop an apraxia of gait. That means they have difficulty knowing how to walk.
Gait dysequilibrium is commonly described as “Doctor, I get dizzy when I walk”. One closing clinical pearl: Physical therapy can often improve gait no matter what the multiple reasons are for failing gait, known or unknown, and so physical therapy is always worth a trial.
Less common but important to recognize is the personality disorder or depression that might cause the patient to complain of “dizziness.” Clues include:
a history of depression, excessive stress, panic attacks or other psychiatric problems. The depressed patient may feel “dissociated” from the world.
When such a patient complains of “dizziness”, it is often hard to pin down exactly what the patient means. Psychiatry should be consulted, and the neuropsychological test called the MMPI can be useful in detecting a tendency toward somatization and in discovering other personality traits.
What is vertigo?
Vertigo refers to an illusion of movement typically described as spinning or whirling. We experienced this as kids when we spun ourselves around and around and then suddenly stopped to watch the world around us continue to spin. Vertigo, however, can also refer to a sense of swaying, for example, in a forward backward direction.
What is true vertigo?
“True” vertigo refers to situations in which this illusion is caused by a disorder of the vestibular system, either peripherally or in its central connections. No one really uses the term “false” vertigo, but there the idea is that the sensation of spinning is due to something other than a dysfunctional vestibular system, such as a psychiatric disorder.
One can recognize vertigo due to vestibular dysfunction by what?
the associated symptoms of nausea and vomiting and by nystagmus.
__________ is the clinical sign of vertigo.
Nystagmus
Describe the phases of nystagmus
It has two components, a fast and a slow phase. The fast phase consists of corrective saccades from the frontal eye field of the contralateral hemisphere. The saccadic eye movement is so quick that the retina cannot process the visual information and a visual blur results. However, the brain suppresses this worthless retinal information and therefore the person is effectively blind during the fast phase of nystagmus.
In contrast to the fast phase, the slow phase of nystagmus is similar in speed to a cortically directed tracking movement, and it is during the slow phase of nystagmus that the person sees during vertigo.
Nystagmus is conventionally described by its fast component. Hence, a right beating nystagmus means that the fast phase is to the right and the slow phase is to the left.
If the eyes are moving slowly from right to the left, in which direction would the room be spinning?
Think about this for a moment. It should be spinning in the opposite direction, namely from left to right. Why is this important?
Before we focus on some disorders of the vestibular system we will review some basic neuroanatomy and physiology underlying the vestibular system.
How many of you have piloted an airplane or steered a sailboat? Those of you who have done so may know that movements in three dimensional space can be described by so-called “degrees of freedom”? What are they and how many are there?
The answer is there are six degrees of freedom that can describe movement in three dimensional space.
Three of these can be considered linear motion along the x, y and z axis. In other words, to get from one point A to another B in space, you can do so by a straight line connecting the two points and the two points can be described by the change in x, y and z axis. The problem is that movement of a ship in space or on the water is also subjected to spins and turns which can be described as rotations about each of the three axes x, y and z. Hence if you spin around the x axis, that is called a “roll”, if you spin around the y axis, that is called “pitch” and if you spin around the z axis, that is called “yaw”. For example, you are walking along a woodland trail looking at the birds in the trees when your foot suddenly catches a tree root and you “pitch” forwards around the y axis.
Let’s take a hypothetical example. It’s summer; you are on the ocean, and your sailboat gets caught in a maelstrom. As you spin and contemplate the many wonders of life you have experienced, you remember from this lecture that the turning movement of the boat could be described as what?
The spinning is called “yaw” and is around the z axis.
The vestibular apparatus in the inner ear is a marvelous sensory device that detects positional changes in all six degrees of freedom and transduces that information into electrical impulses for the vestibular nerve to convey to the brain.
Linear motion and the effects of gravity are sensed by two specialized organs called:
the sacculus and utricle (Other terms are the saccular and utricular maculas). The sacculus lies coplanar with the vertical axis and the utricle lies coplanar with the horizontal axis.
In contrast, the ________ ______ detect angular movements, that is acceleration or deceleration of rotation within the plane of a canal.
semicircular canals (A specialized organ called the cupula located inside the ampulla transduces this information for each semicircular canal. )
Let’s look at the cellular structure of the utricle and saccule. Sensory hair cells with cilia are embedded in a gelatinous matrix. On top of this gelatinous membrane lie tiny crystals of calcium carbonate called otoliths or otoconia. They are stuck to the membrane and are sufficiently heavy to distort the matrix by a linear force during movement and by gravitational forces at all times.
During a change in head position, the plane of the utricle and saccule changes its orientation to gravity and that produces a change in shear stress on the membrane. The direction and degree to which the cilia become deformed results in a proportional increase or decrease of electrical impulses along the vestibular nerve.
So how does the distortion of the hair cell produce a signal?
Like skyscrapers, the cilia are not all of the same height. The tallest cilia is called the kinocilium and depending on how it is bent, potassium channels in the tips of the other cilia either open or close.
The cilia project into endolymph that is rich in potassium. The potassium influx depolarizes the cell membrane which then activates calcium channels that open only when the membrane is depolarized.
The influx of calcium has multiple effects on intracellular metabolism. Namely:
Note that calcium concentration inside the cell is 104 times lower than outside the cell. Hence very little calcium from the outside actually needs to get in to cause a marked increase (10 to 100 fold) in the intracellular calcium concentration.
One effect of the small increase in intracellular calcium rise is to activate calcium dependent potassium pumps that extrude the potassium into the potassium poor perilymph. These counterbalanced activities allow for an electrical resonance of the membrane to shift up or down in frequency and to modulates the concentration of calcium at the hair cell base. A rise in local calcium concentration triggers release of a neurotransmitter as shown on the next slide.
Once again, note that a force directed toward the kinocilium as shown on the far left opens potassium channels. That in turn increases the intracellular calcium concentration triggering more neurotransmitter release, either aspartate or glutamate. The excitatory neurotransmitters activate the afferent fibers from Scarpa’s ganglia. As more neurotransmitter is released, the firing rate of the vestibular nerve fibers increases.
Note that if the force is applied in the opposite direction as shown on the far right, potassium channels close, the cell membrane hyperpolarizes, intracellular calcium falls, less neurotransmitter is released and the frequency of impulses along the vestibular nerve becomes very low.
Here is another look at the same process. The motion detectors consist of hair cells that depolarize when the cilia are deflected in one direction (toward the kinocilium). The depolarization activates sensory nerve fibers at the hair cell’s base. These nerve fibers are the afferent half of bipolar neurons, whose cell bodies lie in Scarpa’s ganglion, and whose efferent axons project to the brainstem via the vestibular nerve.
There is yet another principle to the cellular organization of the hair cells in the utricle and saccule.
Let’s start with the utricle.The orientation of the hair cells are highly organized so that the kinocilium faces a midline valley called the striola. Note the mirror-like arrangement. Also note that the orientation curves by 90 degrees so that every movement in a two dimensional plane will be covered.
With the head in a neutral position looking forward, the utricle is coplanar with the ground. If one tilts the head, the gravitational force will distort the otoconia as shown. Note the mirror orientation of the kinocilia across the striola (that is how the arrows are pointed).
Unidirectional pressure will increase firing on one side (where cilia potassium channels open) and decrease it on the other (where the same channels close). If the applied pressure lies 90 degrees or at a right angle to the kinocilia, the cilia neither open nor close the K+ channels and there is no change in the baseline firing rate. Note that two kinds of forces will alter the firing rate here. A linear force within the plane of the utricle and a static gravitational force when the plane is tilted. The utricle does not transduce rotational forces which is left to the semicircular canals.
Note that the utricle has its kinocilia oriented toward the striola while the saccule has its kinocilia oriented away from the striola. Why the difference exists in the two organs is not clear.
The saccule, also called the sacculus, lies coplanar with the vertical axis. If you stand perfectly still inside an elevator that starts to move up, the lower part of the saccule will be activated because the increased force will be directed toward the kinocilium and that will open the potassium channels. Its mirror upper half will be proportionately inhibited. When the elevator moves down, the exact opposite should occur.
Note that for both the utricle and saccule, the orientation of the kinocilia covers all vectors within an x y plane. In other words, the hair cells show a gradual 90 degree change in orientation so that some will be stimulated and inhibited maximally while others not at all with any linear head movement or with any tilt of the head.
We will next discuss the ampulla and its cupula serving the semicircular canals. One important distinction from the saccule and utricle is that the kinocilia comprising the hair cells of the cupula inside the ampulla always point in one direction only.
Note that the hair cells in the ampulla are oriented in one direction.
A rotational movement within the plane of a semicircular canal will cause the endolymph to flow in one direction or the other. That displaces the cupula and results in depolarization or hyperpolarization of the hair cells. Note also that there are no otoliths stuck on top of these hair cells.
How does the vestibular system affect eye movements?
Note that a net increase in firing from the left vestibular apparatus via Scarpa’s ganglion causes the eyes to move to the right. The red plus indicates activation and the black negative sign indicates inhibition.
One simple way of thinking about this is that each vestibular apparatus acts as a “pushing muscle” directing the eyes to the center. If one side becomes weakened, the normal side will push the eyes toward the weaker side much like the hemiparetic tongue deviates toward the weaker side on protrusion.
If the head is suddenly turned to the left, the left horizontal semicircular canal will be stimulated and the right canal will be inhibited. That will mediate a reflex movement of the eyes to the right so that the point of visual fixation is maintained. This is called the vestibulo-ocular reflex or VOR. It will be addressed later in this module.
Once more, note that movement of endolymph in the canal can cause either a stimulatory or an inhibitory response, depending on the direction of motion and cupula displacement.
Note that the cupula forms an impermeable barrier across the lumen of the ampulla. Free floating otoconia broken off the utricle due to trauma, infection or normal aging, may enter the semicircular canal. To get out, they must exit the same way they entered (away from the ampulla and toward the utricle).
Think for a moment, what effect would gravity have on these dislodged otoliths during sleep and how would that influence endolymphatic flow with head movements? If you said that they would collect in the lowest point of a canal and obstruct flow, that is correct. Since most people sleep on the backs of their heads, the posterior semicircular canal would be the most likely to become obstructed.
So back to true vertigo. It is the illusion of movement due to disease of the vestibular system and/or its pathways. The clinical sign of vertigo is nystagmus, and it is generated as shown.
Note that the information that you have learned about the vestibular system can be used to diagnose psychogenic coma. How can this be done?
Ice water calorics. Ice water in the external auditory canal reduces the temperature of the inner ear by a few degrees but that is enough to cause a drop in the tonic vestibular firing rate. The other, non-irrigated, side continues to fire at a baseline rate but now the two sides are unequal.The normal side pushes the eyes toward the side of ice-water irrigation.
If the patient is in true coma and is disconnected from an otherwise intact brainstem, then the conjugate eye deviation toward the irrigated side is the response to the ice water caloric testing. The picture on the right shows what happens in a coma patient whose brainstem is intact. However, if the patient is awake, the cortex recognizes a mismatch between the vestibular information and other sensory input about where the position of the head is in space. It directs the eyes to get back in the midline by sending down corrective saccades from the frontal eye fields and so the eyes develop a fast beating nystagmus away from the side of irrigation. In other words, you can “rule in” psychogenic unresponsiveness as the cause of coma by demonstrating that ice water in either ear induces nystagmus. This is a Board question that often comes up in Internal Medicine and in Neurology.
The brain does use visual fixation as part of the healing process. How can you tell whether a vestibular imbalance has been compensated over time?
How can you tell if a vestibular imbalance has been compensated by the CNS over time?
One way is to use Frenzel lenses to eliminate visual fixation. These are thick lenses that magnify the eyes and vision is completely blurred. Small lights inside the glasses illuminate the eyes so you can see them better. The next slide shows a video clip of Ménière’s disease in which the Frenzel lenses block visual fixation and unmask a compensated nystagmus.
Now let’s move on. In your approach to the dizzy patient, what do you look for in your history and physical exam?
You first characterize the dizziness including its time course, what triggers it, what effect positional changes have, and whether there are other associated symptoms. A review of systems should be especially comprehensive for the otologic, cardiologic, psychiatric and neurological systems. A drug history is very important for adverse effects on orthostatic blood pressure, gait and balance and feeling drugged or giddy.
The physical exam needs to document whether blood pressure and pulse change with changes in body position. The heart needs careful auscultation looking for evidence of aortic valve stenosis, cardiac failure, arrhythmia, tamponade and so on. Vision should be checked for acuity and double vision ruled out. The motor exam should be carefully performed to look for weakness, spasticity, extrapyramidal dysfunction such as cerebellar ataxia and basal ganglia disease such as parkinsonism. A careful neuro-otological exam should be performed.
How else can you stimulate the horizontal canals at the bedside?
There is a test called the Head Shaking maneuver.
Ask the patient to tilt his or her head down by about 30 degrees. This alligns the horizontal canals coplanar with the ground. Ask the patient to turn the head side to side as quickly as possible for 20 seconds and then stop. This is ideally done with Frenzel lenses so that the patient cannot suppress the nystagmus with visual fixation.
Before we move on to the Dix-Hallpike maneuver, let’s try a mental exercise. Look straight ahead. Now imagine in your mind the orientation of the semicircular canals. How are the two-dimensional planes defined by each canal related to each other on the same side and on the other side of the head?
The semicircular canals detect angular acceleration in 3 planes that are perpendicular to each other. Note again that the horizontal canals lie about 30 degrees above the plane of the ground. The anterior and posterior canals are oriented at right angles to each other. Note that each semicircular canal has a partner on the other side that lies in the same plane:
Right posterior – Left anterior (asterisks),
Right anterior – Left posterior,
Right horizontal – Left horizontal.
Each pair of canals works in a push-pull manner. When head rotation stimulates one, the other partner canal is inhibited.
We now come to a disorder that is perhaps as common as migraine. It is the disorder for which the Dix-Hallpike maneuver is available for making the diagnosis. I am referring to benign paroxysmal positional vertigo or BPPV. Some individuals call it simply benign positional vertigo. What causes BPPV?
The otoconia embedded in the utricle break free of the gelatinous membrane with age or with trauma. Since the posterior semicircular canals are the ones most dependent during sleep, these displaced particles tend to collect in one or both canals. T
hey form a sludge that can plug up the canal lumen so that when the head movement involves the affected posterior canal, there is a sump-like action that produces greater pressure than normal. That causes a greater distortion of the cupula in the ampulla and the canal signals the brain that the head has rotated posteriorly faster and to a greater extent than it really has. The result is vertigo that typically starts 5 to 10 seconds after the head movement and then lasts for 30 to 45 seconds.
BPPV is by far the most common cause of vertigo especially in the elderly.
The condition is usually benign, self-limited and will disappear after a week or two. Occasionally it is protracted and disabling with nausea and vomiting.
The classic complaint is of vertigo when the patient first rolls his head on the pillow in the morning. Vertigo is often triggered when an individual looks up reaching for a high shelf or when changing a ceiling light bulb. Some patients develop vertigo when they look down to tie their shoes.
One neurosurgeon complained that the world would start to spin whenever she looked down into her operating microscope. One elderly patient with dementia could not describe vertigo but said that whenever he stood up, he felt he was “going to die”. In 90% of these patients, the canalith repositioning maneuver can immediately cure the patients of their symptoms.
In some instances, the particles that cause BPPV can actually reach the cupula and cause a distortion there. This is called cupulolithiasis and is considered to be a less common cause of BPPV. On the right you can actually visualize the chalky sludge in the posterior semi-circular canal with an operating microscope.
Okay, so let’s look at some cases. An 86 year old woman with diabetes was admitted for dehydration after nausea and vomiting for one month. She complained of a spinning sensation on sitting up from her bed that would last 1-2 min and cause nausea. The exam showed no orthostatic BP changes. The otologic, cardiovascular and abdominal exams were negative. She had an early Parkinson’s rest tremor but otherwise her neurological exam was negative. The Dix-Hallpike maneuver was positive with head down and to right.
This is a classic example of vestibular neuritis. It is postulated to be due to a viral infection, possibly herpes, similar to what happens in Bell’s palsy. If the cochlea is affected as well, the term labyrinthitis is used. Since the entire vestibular apparatus is inflamed, the motion detectors don’t work for any direction and that allows the other intact vestibular system to function unopposed. Hence movement in any direction is poorly tolerated. Note that shutting down the normal vestibular apparatus with ice water calorics brings temporary relief.
Patients are treated with anticholinergic drugs such as a scopalamine patch and meclizine to suppress the normal vestibular system for symptomatic relief. However, the greater the suppression, the more slowly central compensation restores balance to the unequal vestibular inputs.
Steroids can help recovery.
It is essential that you are not fooled by an acute cerebellar stroke that can produce virtually an identical clinical picture, especially when limb ataxia is not that obvious. Head thrust will be normal in cerebellar stroke but disclose catch-up saccades in vestibular neuritis. The patient, however, will probably not tolerate head movements and refuse to cooperate. CT and MRI can exclude an acute cerebellar stroke.
