Previous post...what is syncope

Thanks to all who responded. I had a pacer put in 2 years ago for severe bradycardia (less than 20 BPM), significant sinus pauses, and 4 episodes of asytole in less than 1 hour. I have a little trouble with dizziness still, sometimes, but was a little surprised by the sudden drops in BP. They did say the pacemaker was keeping my heart rate from dropping too low, so that is why I was wondering about syncope. I just know it (the drop in BP) is a horrible feeling while it is happening (as I am sure most of you have probably experienced). I am glad I was at the hospital during one of the episodes, as my heart was being monitored when it happened. So, even though I thought I was dying (!).....I knew that my pacer was doing what is was supposed to do...!! I

5 Comments

Syncope...

by chip - 2008-12-28 05:12:02

Hello – Sorry to hear that you’re having trouble with syncope!

I’ve had a real problem with it for some time now. Mine has pretty much been controlled by two meds Fludrocortisone and Midodrine along with my knowing how to react to the feeling.

If you are lucky enough to get a warning that an episode is coming on – sit down no matter where you are. In some cases you’ll need to lie flat to get it to pass.

Ask your doctor about the meds, they really do help once you get the dose adjusted.

The American Heart Association has a good deal of information on their site at: http://www.americanheart.org/presenter.jhtml?identifier=4749

Good luck and May God Bless

My Syncope controlled with Pacemaker

by bowlrbob - 2008-12-28 09:12:08

As i posted earlier I was passing out and getting dizzy. My EP turned on the rate drop response on my pacer. I have not had an episode since. I sent you a private mail if you want more info mail me back. The pacer can do it without drugs sometimes. Mine did for the last 3 years. Bowlrbob BOB

Syncope #3

by Pookie - 2008-12-29 02:12:03

Posted by Pookie on 2008-10-08 20:08

Hi again everyone.

I'm in the research and share mood!

BEWARE: VERY LONG POSTING.
(but probably the most informative I've ever found)

(People should consult their doctor before trying any treatment)


GENERAL INFORMATION ON NEURALLY MEDIATED HYPOTENSION AND ITS TREATMENT


What is neurally mediated hypotension?

Neurally mediated hypotension is also known by the following names: the fainting reflex, neurocardiogenic syncope, vasodepressor syncope, the vaso-vagal reflex, and autonomic dysfunction. Hypotension is the formal medical term for low blood pressure, and syncope is the term for fainting. Neurally mediated hypotension occurs when there is an abnormal reflex interaction between the heart and the brain, both of which usually are structurally normal.


When does neurally mediated hypotension lead to symptoms?

Neurally mediated hypotension occurs in susceptible individuals in the following settings:

* after prolonged periods of quiet upright posture (such as standing in line, standing in a shower, or even sitting up for long periods),

* after being in a warm environment (such as in hot summer weather, a hot crowded -corn, a hot shower or bath),
immediately after exercise,

* after emotionally stressful events, (seeing blood or gory scenes, being scared or anxious).

* some individuals get symptoms soon after eating, when blood flow has shifted to the intestinal circulation during the process of digestion.


We are all susceptible to activation of the vaso-vagal reflex that results in a lowered blood pressure (NMH), but each person's susceptibility is affected by his or her genetic make-up, dietary factors, psychological make-up, and acute triggers such as infection and allergy. The clinical problem of NMH occurs when there is sufficiently early triggering of this reflex to cause symptoms.

How does upright posture lead to these problems?

After a normal individual stands up, blood pools in the legs through the effect of gravity. To compensate for the lower amount of blood returning to the heart immediately after standing, the body has a surge of adrenaline (epinephrine). This adrenaline surge leads to a faster heart rate and to more vigorous heart beats (a familiar feeling we all-experience when we are frightened, for example). The faster heart rate and more vigorous heart contractions allow the reduced amount of blood returning to the heart to be pumped more efficiently to vital organs (especially the brain).

In individuals with neurally mediated hypotension, there is a "miscommunication" between the heart and the brain. Just when the heart needs to beat faster, (to pump blood to the brain and prevent fainting), the brain sends out the message that the heart rate should be slowed down, and that the blood vessels in the arms and legs should dilate. These actions take even more blood away from the central part of the circulation where it is needed. In response, individuals feel lightheaded or may faint because not enough blood is getting to the brain. Fainting is helpful, in that it restores a person to the flat position, removing the pooling effect of gravity on the blood, and allowing more blood to return to the heart. Following the lightheadedness or syncope, most individuals feel tired and their mental abilities are somewhat foggy.



Which symptoms can be caused by the neurally mediated hypotension?

Recurrent lightheadedness and fainting are common symptoms, as is an unusual difficulty with prolonged fatigue after a modest amount of physical activity. This post-exertional fatigue can last 24-72 hours, and interferes with many daily activities.

Also observed is chronic fatigue, muscle aches (or fibromyalgia), headaches, and mental confusion which can be prominent symptoms of neurally mediated hypotension even in individuals who do not faint. The mental confusion takes the form of difficulty concentrating, staying on task, paying attention, or finding the right words. Some describe being in a "mental fog." It appears that as long as the fainting reflex is activated whenever the person stands or sits upright for a period of time, then the blood pressure is improperly regulated, and these symptoms are the result. Some develop worse fatigue after such activities as reading and concentrating, and this may be due to the fact that for some, the veins of the arms and legs dilate, thereby allowing more blood to pool, rather than constricting in response to mental tasks.



How is neurally mediated hypotension diagnosed?

Neurally mediated hypotension cannot be detected with a routine blood pressure or heart rate screening. The diagnosis can be made using a prolonged standing test or more commonly using a tilt table test. Many hospitals and academic centers throughout the world perform tilt table testing. It allows careful measurement of the heart rate and blood pressure responses to the head-up position at a 70-degree angle, in an almost standing position. The usual reason for performing a tilt table test in the past had been for the evaluation of recurrent fainting. Many people with neurally mediated hypotension develop adaptations to keep from fainting, such as crossing their legs, fidgeting, or sitting or lying down when they get lightheaded or tired, but the tilt table test prohibits them from performing those natural defences. As a result, lightheadedness, nausea, and fainting often occur during the tilt table test. Fatigue and malaise often occur for a few days after the test is performed.



What causes neurally mediated hypotension?

The answer to this question isn't well understood at present, but it is suspected that neurally mediated hypotension has genetic origins in many people, because it is not uncommon to find several individuals with neurally mediated hypotension in the same family. No gene for this condition has been identified. It is likely that we all could develop neurally mediated hypotension provided that the conditions were sufficiently severe: for example, if we did not take in enough fluids or salt, were subjected to extremely prolonged periods of upright posture, or to very warm environments. The reflex response which results in lowered blood pressure simply occurs at an earlier point in some individuals.

One of the most common, and treatable problems identified in those with neurally mediated hypotension is a low salt (sodium) intake in the diet. Salt helps us retain fluid in the blood vessels, and helps maintain a healthy blood pressure. Salt has received bad press in the last couple of decades because a high salt diet in some individuals with high or high-normal blood pressure can contribute to further elevations in blood pressure, and thereby to heart disease and stroke. This has led to general health recommendations to "cut down on salt." This general recommendation isn't right for all people.

An average adult blood pressure is 120/70, and a blood pressure is considered elevated if it is above 140/90. Individuals can have neurally mediated hypotension at a wide range of resting blood pressures. It may be slightly more common in those whose systolic blood pressure [the top number] is in the 90-110 range, but we also see it in those whose resting blood pressure is high. For individuals with neurally mediated hypotension, a low salt intake may be unhealthy, and may move them from feeling good to developing the symptoms of fatigue and lightheadedness described earlier.


How is neurally mediated hypotension treated?

Neurally mediated hypotension is most often treated with a combination of increased salt and water intake in conjunction with drugs that regulate blood pressure. Some drugs work by allowing the kidneys to retain sodium and others block the body's response to adrenaline, which can kick-start the blood pressure abnormality. In addition, it is important to review your current medications with your doctor to ensure that these medications do not include drugs or vitamins that have the potential to make neurally mediated hypotension worse.

The treatments require persistence, commitment and the willingness to try several possible drugs and combinations over an extended period of time. Because there is a risk of serious side effects with some of the drugs such as elevated blood pressure, elevated sodium levels, lowered potassium levels, or depression, careful monitoring by a physician is required. Among the drugs that have been found to help improve tilt table responses in patients with NMH are fludrocortisone (Florinef), beta-blockers (e.g., atenolol), disopyramide (Norpace), fluoxetine (Prozac), sertraline (Zoloft), ephedrine, pseudoephedrine, theophylline, methylphenidate (Ritalin), and midodrine. Your treating physician should work with you to determine the best possible combination for your personal situation. In general, however, the first step in treating this problem is to increase fluid intake. This cannot be stressed enough.

For some mildly affected individuals, an increased intake of salt and fluids may be all that is needed. Most of those with chronic fatigue syndrome and more severe symptoms require one of several medications in addition to the increased salt and fluid intake. The increased salt and fluid intake continue regardless of which of these medications is added.

To be successful, though, the increased salt intake must be accompanied by a sufficient increase in the intake of water and other fluids (minimum of 2 liters of fluid per day).


Does treatment cure the problem?

It needs to be emphasized that, when successful, the medications for neurally mediated hypotension do not cure the problem. Rather, they help control symptoms. When medications are stopped and when salt intake is reduced, symptoms frequently reappear. Many of the adolescents and adults with the problem also have symptoms resurface or worsen at busy or stressful times (making an oral presentation in class, having company over for Thanksgiving, rushing for a meeting on a hot day and forgetting to drink). Many women describe a worsening of symptoms in the days around the start of a menstrual period.

The question of what happens over the long term has not been adequately studied, and the optimal duration of medical treatment is still being worked out. Unfortunately, despite appropriate doses of the available medications for neurally mediated hypotension, some individuals with abnormal tilt table tests do not experience an improvement in symptoms, and some are intolerant of the medications. This emphasizes the need for more research on this problem. Many women who have NMH describe an improvement in symptoms when they have been pregnant, and often describe pregnancy as the time when they felt "the best ever." The improvement may be due to an expansion of blood volume that occurs with pregnancy.



What other things can I do to get better?

Where practical, avoid circumstances which might bring on symptoms. For example, shop at non-peak hours to avoid long lines. Take shorter showers and baths and aim for a cooler water temperature. Avoid saunas, hot tubs, and lying on a hot beach. Avoid standing still for prolonged periods in hot environments, and on very hot days. Flex your legs muscles and shift your weight when you are standing still. You may also want to avoid alcohol because it often leads to dilation of the veins, and this can "steal" blood away from the central circulation. Most with neurally mediated hypotension are quite intolerant of alcohol. Caffeine intake (including caffeine in soft drinks) affects some people with NMH in an adverse way, so examine whether caffeine is helping you or making symptoms worse.

Certain postures and physical maneuvres are helpful in raising blood pressure when sitting for a prolonged time, mainly by helping use contraction of the leg muscles to pump blood back to the heart and by compressing the abdomen to reduce the amount of blood that pools in the intestinal circulation. adequate blood flow to the brain.

The helpful manoeuvres include:

with one's legs crossed
squatting
standing with one leg on a chair
bending forward from the waist (such as leaning over a shopping cart)
sitting in the knee-chest position
sitting in a low chair
leaning forward with hands on the knees when sitting.

Some of these are less conspicuous than others. Sitting in a low chair (such as a camping stool) is helpful because it causes the legs to be brought up toward the abdomen, and probably reduces the amount of blood pooling in the intestinal circulation. For similar reasons, avoid sitting in a high chair with the legs dangling freely, as there is no resistance to blood pooling unless the muscles are actively contracting. One young woman found she could sit longer without symptoms if she put her feet on a low foot rest (this probably required more leg muscle contraction than regular sitting, and may have also compressed the abdomen better).

Elevate the head of the bed slightly by 10- 15 degrees, a position that appears to help the body retain fluid at night rather than lose fluid into the urine. Depending on one's level of comfort with this form of dress, waist-high support hose can prevent some of the excessive pooling of blood in the legs (knee-high support socks may not work as well), as can garments that increase abdominal compression (these work by preventing excessive amounts of blood pooling in the intestinal circulation).

Exercise is important in regaining the effects that fitness brings in counteracting NNM. Because exercise can make NMH symptoms worse in the period before effective treatment of the NMH has been found, it must be done carefully at first. When you and your doctor feel you are ready, begin a regular regimen of exercise, finding something that does not make you lighthearted and doing it for brief periods at first, increasing gradually but relentlessly. For example, one girl who had been ill for several years began doing better once two of the NMH medications were working for her. She began on a treadmill, but this made her lighthearted, so she switched to a reclining exercise bike. Although she started with only 2 minutes a day, she increased this in small increments and was up to 30 minutes 3 times a week after about three months. Remember to warm up slowly before, and cool down gradually after exercise.


Again, a key part of the therapy is to increase fluid intake. Those who force themselves to drink extra fluids every couple of hours seem to do better than those who aren't as serious about increasing their fluid intakes. Keep in mind that prolonged periods of sleeping (more than 12 hours) may interfere with your ability to attend to your fluid needs on as regular a basis as would be ideal.

Okay, that's it.

Very helpful for people with this diagnosis!!!

Pookie


Syncope #2

by Pookie - 2008-12-29 02:12:24

Posted by Pookie on 2008-11-16 20:47

Found this at www.hrtcare.com

Neurocardiogenic Syncope

Syncope (fainting) is one of the most common medical ailments encountered in clinical practice. Although frequently thought of as a condition with a neurological origin, it’s actually a cardiovascular problem - as such, a neurologic work-up is seldom rewarding. The two main causes of syncope are cardiac arrhythmias and neurocardiogenic (vasovagal, vasodepressor) syndromes. In both of these conditions, blood circulation to the brain is reduced, resulting in temporary loss of consciousness.


Among the arrhythmias causing syncope, tachycardias (fast heartbeats), particularly those of ventricular origin, rather than bradycardias (slow heartbeats) are more often the culprits. In most patients with any evidence of previously known heart disease, it is likely that their syncope is related to a cardiac arrhythmia, usually VT. This is a serious matter because in patients with syncope due to VT, it’s common for SCD to occur within the ensuing year, this should be preventable if the cause of the syncope is found and managed. All cardiac arrhythmias can be effectively controlled if proper diagnosis is made with the help of cardiac electrophysiologic studies. In general, if a slow heart beat is the problem it can be treated with a pacemaker. If rapid beating is discovered, the treatment will vary depending on the nature of the fast rhythm.


Another common cause of syncope/presyncope is neurocardiogenic (vasovagal) syndrome. This condition, known by physicians as "neurally mediated hypotension", is also referred to as "the fainting reflex", "vasodepressor syncope", "vasovagal syncope", or "autonomic dysfunction". In this condition blood vessels tend to expand, which leads to pooling of blood in the lower parts of the body. As a result, less blood reaches the brain and this causes fainting. The usual stimulus for this action resides in the nerves of the heart-hence the term neurocardiogenic. A head-up tilt test can uncover the underlying cause of the fainting in this syndrome. Neurocardiogenic syncope is usually treated with medications that reduce the probability of cardiac nerves triggering the cycle that leads to lightheadedness, dizziness or fainting.


Together, arrhythmias and neurocardiogenic syndromes account for more than 75% of the cases of unexplained fainting spells-so it’s important that the initial diagnostic work-up be designed to investigate these possibilities.


When Does Neurocardiogenic Syncope Lead to Symptoms?

Neurocardiogenic syncope occurs in predisposed individuals in the following settings:


after prolonged periods of quiet upright posture (such as standing in line)


after being in a warm environment (such as in hot summer weather, a hot crowded room, a hot shower or bath)


immediately after exercise


after emotionally stressful events (having blood drawn, being scared or anxious)

some individuals get symptoms soon after eating, when blood flow has shifted to the intestinal circulation during the process of digestion


We are all susceptible to fainting by activation of the vaso-vagal reflex that results in a lowered blood pressure, however, an individual’s susceptibility varies day to day based upon genetic make-up, dietary factors, psychological state, and triggers such as infection, dehydration, and alcohol intake.

Why Does an Upright Posture Trigger Neurocardiogenic Syncope?

When a normal individual stands up, gravity causes blood to pool in the legs, and return of blood to the heart is decreased. In order to compensate for this reduction, the body releases a surge of adrenaline (epinephrine). The heart beats faster and more forcefully, thereby pumping blood more efficiently to vital organs (especially the brain).


In an individual with neurocardiogenic syncope, the reduction of blood return triggers a miscommunication between the heart and the brain. Just when the heart needs to beat faster, the brain sends out a message that the heart rate should be slowed down, and that the blood vessels in the arms and legs should dilate. These actions take even more blood away from the central part of the circulation where it is needed. As a result, the individual feels lightheaded or may faint because not enough blood is getting to the brain. Fainting is helpful, in that it restores a person to the flat position, removing the pooling effect of gravity on the blood, and allowing more blood to return to the heart. Following the lightheadedness or syncope, most individuals feel tired and their mental abilities are somewhat foggy.

What Symptoms Does Neurocardiogenic Syncope Cause?

Individuals that are prone to neurocardiogenic syncope manifest a spectrum of symptoms ranging from fatigue, vague lightheadedness, recurrent dizziness, near fainting, palpitations, nausea, unexplained sweating, joint or muscle aches, to the most dramatic "the faint". Some people may only have one or more of these symptoms but never progress to fainting. Prolonged fatigue after a modest amount of physical activity is occasionally seen. This post-exertional fatigue can last 24-72 hours, and interferes with many daily activities.


Some develop worse fatigue after such activities as reading and concentrating, and this may be due to the fact that for some, the veins of the arms and legs dilate, thereby allowing more blood to pool, rather than constricting in response to mental tasks.

How is Neurocardiogenic Syncope Diagnosed?

Neurocardiogenic syncope cannot be detected in the office with a routine blood pressure or heart rate screening. The diagnosis can be made using a tilt table test. Since heart rate and blood pressure recordings are impractical during an actual episode, a test designed to provoke this episode in a controlled setting is used. A tilt table test allows careful measurement of the heart rate and blood pressure responses to the head-up position at a 70-degree angle, in an almost standing position.


Many people with neurocardiogenic syncope develop adaptations to keep from fainting, such as crossing their legs, fidgeting, or sitting or lying down when they get lightheaded or tired, but the tilt table test prohibits them from performing those natural defenses. As a result, lightheadedness, nausea, and fainting can be provoked during the tilt table test. Fatigue and malaise may occur for a few days after the test is performed. The test itself is safer than the actual episode in real life because the event is monitored carefully.

What Causes Neurocardiogenic Syncope?

The cause for neurocardiogenic syncope isn't well understood at present, but we suspect this condition has genetic origins in many people, because it is not uncommon to find several affected individuals in the same family. It is likely that we all could develop this neurally mediated drop in blood pressure provided that the conditions were sufficiently severe: for example, if we were dehydrated, were subjected to extremely prolonged periods of upright posture, or to very warm environments. The reflex response, which results in lowered blood pressure, simply occurs more easily and without an apparant trigger in susceptible individuals.


One of the most common and treatable problems identified in those with neurocardiogenic syncope is a low salt (sodium) intake in the diet. Salt helps us retain fluid in the blood vessels, and helps maintain a healthy blood pressure. For individuals with neurocardiogenic syncope, a low salt intake may move them from feeling good to developing the symptoms of fatigue and lightheadedness described earlier.

How is Neurocardiogenic Syncope Treated?
Neurocardiogenic syncope is most often treated with a combination of increased salt and water intake in conjunction with drugs that regulate blood pressure. It is important for patients to recognize potential triggers and heed warning signs. Treatment can broadly be divided into two categories:


1. General measures
2. Medications


General Measures:


The first step in treating this problem is to increase fluid intake. We cannot stress this enough. Patients who drink fluids regularly throughout the day seem to do better than those who don't take this task seriously.


If low salt intake is an issue, we recommend an increase in the amount of salt for patients to add to their food. For some individuals with mild symptoms, an increased intake of salt and fluids may be all that is needed. Most of those with chronic fatigue syndrome and more severe symptoms require one of several medications in addition to the increased salt and fluid intake. The increased salt and fluid intake continue regardless of which of these medications is added. To be successful, though, the increased salt intake must be accompanied by a sufficient increase in the intake of water and other fluids (minimum of 2 liters of fluid per day). Please contact your physician if you have high blood pressure.


Where practical, avoid circumstances that might bring on symptoms.

Shop at non-peak hours to avoid long lines


Take shorter showers and baths and aim for a cooler water temperature


Avoid saunas, hot tubs, and lying on a hot beach


Avoid standing still for prolonged periods in hot environments, and on very hot days

Flex your leg muscles and shift your weight when you are standing still, or better still, walk around.


Avoid alcohol because it leads to dilation of the veins and arteries, and this can steal blood away from the central circulation


Reduce caffeine intake


Certain postures and physical maneuvers are helpful in raising blood pressure when sitting for a prolonged time, mainly by helping use contraction of the leg muscles to pump blood back to the heart and by compressing the abdomen to reduce the amount of blood that pools in the intestinal circulation. The helpful maneuvers include:


standing with one's legs crossed


squatting

standing with one leg on a chair


bending forward from the waist (such as leaning over a shopping cart)


sitting in the knee-chest position


sitting in a low chair


leaning forward with hands on the knees when sitting


elevate the head of the bed slightly by 10-15o, a position that appears to help the body retain fluid at night rather than lose fluid into the urine


waist-high support hose can prevent some of the excessive pooling of blood in the legs (knee-high support socks may not work as well


Exercise is important in regaining the effects that fitness brings in counteracting neurocardiogenic syncope. Because exercise can initially make symptoms worse, it must be done carefully at first.

Medications:


Medications are designed to make the patient more resistant to the same triggers, especially if they cannot be identified or eliminated. Some drugs work by allowing the kidneys to retain sodium and others block the body's response to adrenaline, which can kick-start the blood pressure abnormality. In addition, it is important to review your current medications with your doctor to ensure that these medications do not include drugs or vitamins that have the potential to make neurocardiogenic syncope worse.


The treatments require persistence, commitment and the willingness to try several possible drugs and combinations over an extended period of time. Because there is a risk of serious side effects with some of the drugs, such as elevated blood pressure, elevated sodium level, lowered potassium level, or depression, careful ongoing monitoring by a physician is required. Drugs that have been found to help are:

beta-blockers (e.g., atenolol)


fludrocortisone (Florinef)


disopyramide (Norpace)


fluoxetine (Prozac)


sertraline (Zoloft)

midodrine


ephedrine


pseudoephedrine


theophylline


methylphenidate (Ritalin), and



Your treating physician will work with you to determine the best possible drug or combination of drugs for you.

Does Treatment Cure the Problem?
No, treatment for neurocardiogenic syncope does not cure the problem. Rather, it helps control (minimize if not eliminate) symptoms and is aimed at improving quality of life. When medications are stopped and when salt intake is reduced, symptoms frequently reappear. Many of the adolescents and adults with the problem also have symptoms resurface or worsen at busy or stressful times (making an oral presentation in class). Many women describe a worsening of symptoms in the days around the start of a menstrual period.


The question of what happens over the long term has not been adequately studied, and the optimal duration of medical treatment is still being worked out. Unfortunately, despite appropriate doses of the available medications, some individuals with abnormal tilt table tests do not experience a marked improvement in symptoms, and some are intolerant of the medications. In such people, the realistic expectation may be reduction in frequency and severity of symptoms rather than their complete elimination. More research on this problem is ongoing.


Hope this helps someone.

Pookie

Syncope

by Pookie - 2008-12-29 02:12:29

Posted by Pookie on 2008-12-03 21:38

Just thought it was time for this again...hope it helps even just one member as being dizzy 24/7 is not fun...I know, I live it every day. Yuck.

Hi everyone!

I was doing some research on dizziness here on this website and found the following information. I find it very interesting as a lot of members seem to mention dizziness. Hope this helps.

Dizziness is the second most common complaint heard in doctors' offices (after lower back pain). Dizziness has many causes other than inner ear dysfunction.

Visual disturbances can result in lightheadedness or dizziness. Some people feel dizzy while adjusting to bifocals or a new eyeglass prescription, or from reduced vision due to cataracts.

Hyperventilation can cause temporary dizziness. During rapid breathing, more carbon dioxide than normal is expelled and the level of carbon dioxide in the blood falls, which in turn affects the function of brain cells.

Decreased blood flow to the brain or brain stem can cause dizziness, because insufficient oxygen is reaching the cells. Conditions that can reduce blood flow to the brain include orthostatic hypotension (low blood pressure upon suddenly rising from a lying or sitting position), dehydration, vasovagal syndrome (a nervous-system response that causes sudden loss of muscle tone in peripheral blood vessels), arteriosclerosis (hardening or narrowing of blood vessels), and osteoarthritis (a joint disease that can narrow the openings in the neck vertebrae through which blood vessels flow).

Nervous-system disorders such as peripheral neuropathies (diminished nerve function in the legs or feet) can cause unsteadiness. A tumor may affect the brain stem, the cerebellum (the coordination center of the brain), or the part of the cerebral cortex that controls voluntary muscle movements.

Even stress, tension, or fatigue may cause dizziness. Under these conditions, the brain stem functions less efficiently, resulting in some loss of automatic reflex control of balance. This leads to elevated levels of activity for the cerebral cortex, as conscious energy is used to help maintain balance by controlling voluntary muscle movements. Lightheadedness and unsteadiness can result.

Pookie

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