Migraine (or Headaches) and Vertigo (or Dizziness): Top 10 causes? And What to Do About Migraine with Vertigo.

Top 20 Causes for Migraine and Vertigo 
(or Headaches and Dizziness) 
And What to Do About Migraine with Vertigo.

Sandra Lora Cremers, MD, FACS

Having pain in your head, whether it is a headache or migraine, can be very disconcerting and make life tougher. Adding vertigo or dizziness to the equation can make it hard to work, drive, and function. 

The causes (or differential) for Headaches and Vertigo are similar. A previous post discusses the some of the key causes of headaches and migraines: https://drcremers.com/2014/02/migraine-diet-recommended-and-not.html

If you have Headaches, Vertigo, Racing Pulse, the differential narrows down a bit, with POTS
Postural Orthostatic Tachycardia Syndrome (POTS) (see below) or an Autoimmune Disease (see below) as something that needs to be looked into in particular (my MD friend had this at Harvard and it took years of visits to doctors all over the country to finally get a diagnosis. She had to be intubated as she stopped breathing before they got the diagnosis correct). Still most of the causes below can be the culprit behind Headaches, Vertigo, Racing Pulse. 

The goal to finding the cause will be to rule out all the most common causes and asking your MD to be sure you do not have POTS or an autoimmune disease. 

Let’s start with some definitions:
1. What is Vertigo?  Vertigo is a general term used to describe a sensation that you are spinning or that the world around you is spinning when neither you nor your environment is spinning.
More formally: 
A. Spontaneous vertigo including:

Internal vertigo, a false sensation of self-motion, and
External vertigo, a false sensation that the visual surround is spinning or flowing

B. Positional vertigo, occurring after a change of head position
C. Visually induced vertigo, triggered by a complex or large moving visual stimulus
D. Head motion-induced vertigo, occurring during head motion

E. Head motion-induced dizziness with nausea. Dizziness is characterized by a sensation of disturbed      spatial orientation. Other forms of dizziness are currently not included in the classification of vestibular  migraine.

2. Dizziness is used to describe a range of sensations, such as feeling faint, woozy, weak or unsteady. Dizziness that creates the false sense that you or your surroundings are spinning or moving is called vertigo.
3. Unsteadiness (a sense of imbalance or staggering when standing or walking). This sometimes is called disequilibrium
4. Lightheadedness or feeling as if you are about to faint (pre-syncope; syncope is when you actually faint). This may mean there is a heart problem or low blood pressure.

The Most Common Causes of Vertigo

Some of these causes appear together to cause a “tipping point” of instability. 

1. Dehydration (this is also a leading cause for headaches & a trigger for migraines). Check to be sure you are well hydrated. Note that both migraine and vertigo are common complaints in the general population and may coexist in a patient just by coincidence: true, true but unrelated. 

2. Low Blood Pressure or standing up too quickly (this is also a leading cause for headaches & a trigger for migraines). Check your blood pressure in both arms & legs and at different times of day and with different activities. 

3. Anxiety &/or Stress &/or a sub-optimal Diet(this is also a leading cause for headaches & a trigger for migraines): Most everyone I know is stressed out, so this one is harder to pinpoint. Even in friends who go to daily mass, stress can be an underlying culprit for many ailments: keep working on keeping your inner peace. 
Be aware to change your diet to a low inflammatory diet: https://drcremers.com/2016/04/low-inflammatory-diet.html
Consider a drastic diet, like Dr. Fuhrman’s diet. I am not sure I could truly due that diet now, but my surgical colleague started this diet after he was told he was about to have a heart attack or stroke as his cholesterol was super high (and his father and grandfather both had strokes). 

4. Anemia: Iron-deficiency anemia in particular can cause vertigo and/or headaches. Check your CBC

5. Aging: As we get older our vestibular system of the inner ear, eye muscles may not work as they did before. Any age-related cardiovascular problems can cause vertigo and/or headaches. Not much you can do about this one. Keep praying that your symptoms will resolve. [As an aside: My favorite videos, I must confess, on keeping a optimistic attitude of the power of prayer are: A favorite movie about Padre Pio  https://www.youtube.com/watch?v=SL73fLXqo1k and a video about Venerable Solanus Casey we found on Formed.org (our favorite family video website).]

6. Inner Ear Problems: Any inner ear problem can cause vertigo. Vertigo is often caused by an inner ear problem. Some of the most common causes include:

7. Ear Infection: usually one has pain and/or a fever. This can be easily diagnosed with an otoscope.

8. BPPV. Benign paroxysmal positional vertigo. BPPV occurs when tiny calcium particles (canaliths) clump up in canals of the inner ear: my father in law had this & it almost drove him crazy. A previous blog posts tells more: https://drcremers.com/2014/05/great-review-on-vertigo-dizziness.html
The inner ear sends signals to the brain about head and body movements relative to gravity. It helps you keep your balance.
BPPV can occur for no known reason or it can start after head trauma or just be associated with age.
Also Benign recurrent vertigo (see below) can cause migraines/headaches and vertigo.a
9. Meniere’s disease. This is an inner ear disorder thought to be caused by a buildup of fluid and changing pressure in the ear. It can cause episodes of vertigo along with ringing in the ears (tinnitus) and hearing loss.
10. Vestibular neuritis or labyrinthitis. This is an inner ear problem usually related to infection (usually viral). The infection causes inflammation in the inner ear around nerves that are important for helping the body sense balance.
11. Heart or Cardiovascular issues: aging, blood pressure issues, low or high blood pressure, high cholesterol issues or hardening of the arteries can be a contributing factor to vertigo and headaches. 
12. Medications: Some medications can cause vertigo & meadaches
13. Migraines: Migraines can cause vertigo. Migraines is a broad term which includes many subdivisions. Here is one example.
Diagnostic criteria for migraine without aura
A. At least five attacks fulfilling criteria below
B. Headache attacks lasting 4–72 hours

C.Headache has at least two of the following characteristics:
1.Unilateral localization
2.Pulsating quality
3.Moderate or severe pain intensity
4.Aggravation by or causing avoidance of routine physical activity

D.During headache at least one of the following:
1.Nausea and/or vomiting
2.Photophobia and phonophobia

E.Not attributable to another disorder

The below are less common, but require attention if all the above is normal:
14. Automimmune Diseases
15. Vestibular Migraine (VM): a relatively new term discussed below. Note that new vestibular syndromes have been named to classify a combination of symptoms with no clear blood test but particular findings on exam, such as vestibular migraine (VM), superior canal dehiscence syndrome, and vestibular paroxysmia. 
VM is by far the most common of these new disorders, gaining increasing recognition by clinicians and scientists. 
16. POTS: (see below for more information) 
Postural Orthostatic Tachycardia Syndrome (POTS)
17. Brain problems: from previous trauma, previous inflammation, autoimmune related 
18. Aneurysm
19. Stroke
20. Brain Tumor or Tumor around ear

Symptoms of Vertigo
Vertigo is often triggered by a change in the position of your head.
People with vertigo typically describe it as feeling like they are:
  • Spinning
  • Tilting
  • Swaying
  • Unbalanced
  • Pulled to one direction
Other symptoms that may accompany vertigo include:
  • Feeling nauseated
  • Abnormal or jerking eye movements (nystagmus)
  • Headache
  • Sweating
  • Ringing in the ears or hearing loss
Symptoms can last a few minutes to a few hours or more and may come and go.

Treatment for Vertigo

Treatment for vertigo depends on what’s causing it. In many cases, vertigo goes away without any treatment. This is because your brain is able to adapt, at least in part, to the inner ear changes, relying on other mechanisms to maintain balance.
For some, treatment is needed and may include:
Vestibular rehabilitation. This is a type of physical therapy aimed at helping strengthen the vestibular system. The function of the vestibular system is to send signals to the brain about head and body movements relative to gravity.


Postural Orthostatic Tachycardia Syndrome;

Many years ago, one of my best friends at Harvard Medical School was diagnosed with POTS. She was an attending doctor at Harvard Medical School when her symptoms first started and no one could figure out what she had. Likely some thought she was crazy given the bizarre symptoms, but those of us who were blessed to have her as a friend knew she was not making this up. 

As the doctors at Harvard debated what was causing her symptoms, she started having trouble breathing. Soon she stopped breathing and a friend of hers, the head of Anesthesiology was shocked to see who the patient was: he was paged STAT to intubate his friend and colleague. “Don’t do this to me,” were the last words she heard him say as he had to intubate her, a fellow colleague. Shortly after this episode, and after they ruled out everything under the sun, including Guillain-Barre Syndrome and many viruses, the idea that it could be POTS came up. At that time POTS was not understood and only two center existed: one at the MAYO clinic and one in TEXAS. She went to both. Finally after years of difficulty, she was formally diagnosed with POTS. She started multiple treatments with a high salt diet, and she has been fine ever since (with a few issues along the way, such as having a long recovery time from a virus or cold). 
Here is more information below.
Postural Orthostatic Tachycardia Syndrome (POTS) is a form of dysautonomia that is estimated to impact between 1,000,000 and 3,000,000 Americans, and millions more around the world. POTS is a form of orthostatic intolerance that is associated with the presence of excessive tachycardia and many other symptoms upon standing.1

Diagnostic Criteria
The current diagnostic criteria for POTS is a heart rate increase of 30 beats per minute (bpm) or more, or over 120 bpm, within the first 10 minutes of standing, in the absence of orthostatic hypotension.1,2,3,4 In children and adolescents, a revised standard of a 40 bpm or more increase has recently been adopted.4,5 POTS is often diagnosed by a Tilt Table Test, but if such testing is not available, POTS can be diagnosed with bedside measurements of heart rate and blood pressure taken in the supine (laying down) and standing up position at 2, 5 and 10 minute intervals. Doctors may perform more detailed tests to evaluate the autonomic nervous system in POTS patients, such as Quantitative Sudomotor Axon Reflex Test (QSART, sometimes called Q-Sweat), Thermoregulatory Sweat Test (TST), skin biopsies looking at the small fiber nerves, gastric motility studies and more.

Signs and Symptoms
While the diagnostic criteria focus on the abnormal heart rate increase upon standing, POTS usually presents with symptoms much more complex than a simple increase in heart rate. It is fairly common for POTS patients to have a drop in blood pressure upon standing, but some POTS patients have no change or even an increase in blood pressure upon standing.1 POTS patients often have hypovolemia (low blood volume) and high levels of plasma norepinephrine while standing, reflecting increased sympathetic nervous system activation.3 Approxiamtely 50% of POTS patients have a small fiber neuropathy that impacts their sudomotor nerves. Many POTS patients also experience fatigue, headaches, lightheadedness, heart palpitations, exercise intolerance, nausea, diminished concentration, tremulousness (shaking), syncope (fainting), coldness or pain in the extremeties, chest pain and shortness of breath.1,3,4 Patients can develop a reddish purple color in the legs upon standing, believed to be caused by blood pooling or poor circulation. The color change subsides upon returning to a reclined position.

Quality-of-Life and Disability
Some patients have fairly mild symptoms and can continue with normal work, school, social and recreational activities. For others, symptoms may be so severe that normal life activities, such as bathing, housework, eating, sitting upright, walking or standing can be significantly limited.1,3 Physicians with expertise in treating POTS have compared the functional impairment seen in POTS patients to the impairment seen in chronic obstructive pulmonary disease (COPD) or congestive heart failure.1 Approximately 25% of POTS patients are disabled and unable to work.1 Researchers found that quality-of-life in POTS patients is comparable to patients on dialysis for kidney failure.21, 22

History of POTS
The term “POTS” was coined in 1993 by a team of researchers from Mayo Clinic, led by neurologist Dr. Philip Low.8However, POTS is not a new illness; it has been known by other names throughout history, such as DaCosta’s Syndrome, Soldier’s Heart, Mitral Valve Prolapse Syndrome, Neurocirculatory Asthenia, Chronic Orthostatic Intolerance, Orthostatic Tachycardia and Postural Tachycardia Syndrome.3 In the past, it was mistakenly believed to be caused by anxiety. However, modern researchers have determined that POTS is not caused by anxiety.2,6,7 It is caused by a malfunction of the patient’s autonomic nervous system. Thankfully, in the last 20 years, researchers have gained much more insight into imbalances of the autonomic nervous system.1

POTS Classifications
POTS researchers have classified POTS in various ways. Dr. Blair Grubb has described POTS as “primary” or “secondary.” “Primary” refers to POTS with no other identifiable medical condition (also known as “idiopathic” POTS). “Secondary” refers to POTS with the presence of another medical condition known to cause or contribute towards POTS symptoms.1 Dr. Julian Stewart has described “high flow” and “low flow” POTS, based upon the flow of blood in the patients lower limbs.9

Other researchers have described POTS based on some of its more prominent characteristics: hypovolemic POTS, which is associated with low blood volume; partial dysautonomic or neuropathic POTS which is associated with a partial autonomic neuropathy; and hyperandrenergic POTS which is associated with elevated levels of norepinephrine.1,3,4 These are not distinct medical conditions and many POTS patients have two or three of the different characteristics present. For example, one patient can have neuropathy, low blood volume and elevated norepineprhine.

Who Develops POTS?
POTS can strike any age, gender or race, but it is most often seen in women of child bearing age (between the ages of 15 and 50).2 Men and boys can develop it as well, but approximately 80% of patients are female.2

Is POTS Caused by Anxiety?
While some of the physical symptoms of POTS overlap with the symptoms of anxiety, such as tachycardia and palpitations, POTS is not caused by anxiety. POTS patients are often misdiagnosed as having anxiety or panic disorder, but their symptoms are real and can severely limit a person’s ability to function.1,3 Research has shown that POTS patients are similarly or even less likely to suffer from anxiety or panic disorder than the general public.3,5,6,7 Research surveys that evaluate mental health show similar results between POTS patients and national norms.20

What Causes POTS?
POTS is a heterogeneous (meaning it has many causes) group of disorders with similar clinical manifestations.1,4 POTS itself is not a disease; it is simply a cluster of symptoms that are frequently seen together. This is why the ‘S’ in POTS stands for “Syndrome.” Since POTS is not a disease, it is fair to say that POTS is caused by something else. However, figuring out what is causing the symptoms of POTS in each patient can be very difficult, and in many cases, patients and their doctors will not be able to determine the precise underlying cause. When doctors cannot pinpoint the underlying cause of a patient’s POTS, it may be called Primary or Idiopathic POTS.1 Idiopathic simply means “of an unknown origin.”

While researchers are still working to identify the root causes and pathology of POTS, there are several underlying diseases and conditions that are known to cause or be associated with POTS or POTS like symptoms in some patients. This is a partial list:

-Autoimmune Diseases such as Autoimmune Autonomic Ganglionopathy, Sjogren’s Syndrome, Lupus, Sarcoidosis, Antiphospholipid Syndrome;1,3, 22
-Chiari Malformation19
-Delta Storage Pool Deficiency13
-Diabetes and pre-diabetes
-Ehlers Danlos Syndrome – a collagen protein disorder than can lead to joint hypermobility and “stretchy” veins;3,12
-Genetic Disorders/Abnormalities;3
-Infections such as Mononucleosis, Epstein Barr Virus, Lyme Disease, extra-pulmonary Mycoplasma pneumonia and Hepatitis C;1,2,3,4,10,11
-Multiple Sclerosis;14
-Mitochondrial Diseases;15
-Mast Cell Activation Disorders;3
-Paraneoplastic Syndrome – rare small tumors of the lung, ovary, breast and pancreas that produce antibodies;1
-Toxicity from alcoholism, chemotherapy and heavy metal poisoning.1
-Traumas, pregnancy or surgery;1,2,3
-Vitamin Deficiencies/Anemia;16,17

Each patient is different, thus consulting with a physician who has experience in treating autonomic disorders is important. The most common treatments for POTS include increasing fluid intake to 2-3 liters per day; increasing salt consumption to 3,000 mg to 10,000 mg per day; wearing compression stockings; raising the head of the bed (to conserve blood volume); reclined exercises such as rowing, recumbent bicycling and swimming; a healthy diet; avoiding substances and situations that worsen orthostatic symptoms; and finally, the addition of medications meant to improve symptoms.1,3 Many different medications are used to treat POTS, such as Fludrocortisone, Beta Blockers, Midodrine, Clonidine, Pyridostigmine, Benzodiazepines, SSRIs, SNRIs, Erythropoietin and Octreotide.1,3 If an underlying cause of the POTS symptoms can be identified, treating the underlying cause is very important as well.

Currently, there is no cure for POTS, however researchers believe that some patients will see an improvement in symptoms over time. Detailed long term follow up studies on the course of POTS are sparse, but Dysautonomia International is working with researchers to begin to collect long term follow up data. With proper lifestyle adjustments, exercise, diet and medical treatments, many patients see an improvement in their quality of life.1 If an underlying cause can be identified, and if that cause is treatable, the POTS symptoms may subside. While the prognosis is good for most patients, researchers have noted that some patients will not improve and may actually worsen over time.1

The longest follow-up study done to date comes from Mayo Clinic.20 Mayo Clinic did a survey of their pediatric POTS patients seen between 2003 and 2010. Of those who responded to the survey, 18.2% reported a complete resolution of their POTS symptoms, while 52.8% reported persistent but improved symptoms. Male patients were twice as likely to report recovery. The average survey respondent had been diagnosed for about 5 years. Both patients who fully recovered and those who did not had mental health scores similar to the national norm.


Is a relatively recent (within last 20 years) syndrome, meaning it is a group of symptoms lumped together and has no clear blood work that can label it a disease as of yet.

Similar to migraine, there is no clinical or laboratory confirmation for VM.

How do you diagnosis VM?
It is frustrating as it is a diagnosis of exclusion: this means a patient’s history and complaints plus negative/normal findings on all the other possible causes above.

1. Vestibular migraine

A. At least 5 episodes with vestibular symptoms
1. of
moderate or severe intensity
2. lasting 5 min to
72 hours
B. Current or previous history of migraine with or without
aura according to the International Classification
of Headache Disorders (ICHD)
C. One or more migraine features with at least 50% of
the vestibular episodes
– headache with at least two of the following characteristics:
one sided location, pulsating quality,
moderate or severe pain intensity, aggravation by
routine physical activity

– photophobia and phonophobia
– visual aura
D. Not better accounted for by another vestibular or
ICHD diagnosis

2. Probable vestibular migraine

A. At least 5 episodes with vestibular symptoms of
moderate or severe intensity, lasting 5 min to
72 hours
B. Only one of the criteria B and C for vestibular migraine
is fulfilled (migraine history or migraine features
during the episode)

C. Not better accounted for by another vestibular or
ICHD diagnosis

How does a migraine affects the vestibular system?
No one is sure but there are many theories related to aging, structural changes, hormonal changes, stress & anxiety (a off beat report, but I must include this link as it is a unusual case of one patient: http://www.mvertigo.org/t/the-real-cause-of-mav-and-or-menieres/376

No one has done a high-quality treatment trial as of yet. Thus for VM or Migraine Associated with Vertigo, the goal for now is to treat the underlying migraine.

Differential diagnosis

The differential diagnosis of VM includes other disorders causing episodes of spontaneous and positional vertigo. Again, history taking provides more valuable clues than technical procedures, which rather serve to provide further evidence for or against a clinical working diagnosis.

Menière’s disease

The most challenging differential diagnosis of VM is Menière’s disease, particularly in the early course, when permanent hearing loss may not yet be detectable in the latter. Both disorders present similarly in terms of severity and duration of vertigo episodes and vestibular testing with 
1. Caloric irrigation
2. Head impulse test
3. VEMPs 
do not reliably discriminate between VM and Menière’s disease. 
Usually, the distinction can be made based on hearing loss, which is only occasional and mild in VM, while it is a typical and more severe accompaniment of Menière’s disease. Also hearing loss in VM is usually in both ears but in Menière  pateints, hearing issues in both ears happens in only 2% at the beginning of Menière disease. Again, in contrast to Menière’s disease, in which these symptoms are typically unilateral, these symptoms are usually bilateral in VM 
There is a diagnostic overlap between VM and Menière’s disease, not only in the early stage. 10% of patients fulfilled diagnostic criteria for both Menière’s disease and VM after about 9 years. Yet, these patients had clinical features atypical of classical Menière’s disease, such as symmetric and mostly mild hearing loss and often long duration of vertigo episodes, raising doubts that Menière’s disease was the more appropriate diagnosis .
Current diagnostic criteria for Menière’s disease and VM are not sufficiently discriminative. There may be a genetic link between VM and Menière’s disease
Notes, some MDs think migraine can damage the inner ear, leading to endolymphatic hydrops
Endolymphatic hydrops has been identified in a minority of patients with VM by means of magnetic resonance imaging (MRI), but most of them also fulfilled criteria for Menière’s disease.
Note, migrainous symptoms such as headache and photophobia are also frequent accompaniments in attacks of Menière’s disease 
When patients present with early unilateral hearing loss and vertigo attacks lasting at least 20 minutes and not longer than 12 hours, Menière’s disease should be diagnosed, even when migraine symptoms occur during vertigo episodes. 
In those patients with only minor hearing symptoms and a history compatible with both VM and Menière’s disease, medical treatment with a trial of migraine prophylaxis is advisable. 
Avoid invasive procedures till a more definite diagnosis is made. Only patients who have two different types of attacks, one fulfilling the criteria for VM and the other for Menière’s disease, should be diagnosed with the two disorders and afuture classification of VM may include a VM/Menière’s disease overlap syndrome.

Benign recurrent vertigo

The term “benign recurrent vertigo” means you have recurrent attacks of spontaneous vertigo that cannot be explained by other known peripheral or central vestibular disorders.  There is a large overlap between benign recurrent vertigo and VM. 
Benign recurrent vertigo and VM are similar in that
1. Both can occur with migraines
2. Female preponderance 
3. Genetic: Family occurrence suggestive of an autosomal-dominant inheritance, 
4. Precipitation by lack of sleep and emotional stress 
5. Transition from spontaneous to positional vertigo during an episode 


Treatment of VM starts with effective counseling. 
One has to understand a bit the complexity of why migraines happen and be sure all MRIs & blood tests are normal. This will help relieve the fear of a slow painful death as there are many medicines that can help you return to a normal life. 
No drug approaches to the prophylactic treatment of VM can be as effective as medication. Avoidance of identified triggers, regular sleep and low inflammatory (ideally no gluten or sugar) meals, and physical exercise are key to prevent any migraine.
In migraine headaches, relaxation techniques and biofeedback are as effective as pharmacologic prophylaxis.
Symptomatic treatment during episodes of VM lasting longer than 1 hour can be achieved with vestibular suppressants such as dimenhydrinate. 
There is anecdotal evidence that triptans may be effective for VM. The only controlled trial on the efficacy of triptans in VM remained inconclusive due to its limited power. A retrospective study found that the effect of triptans on vertigo was related to its effect on headache. Interestingly, triptans seem also to reduce motion sickness in those with migraines, possibly by influencing serotonergic vestibuloautonomic projections. 
Intravenous methylprednisolone (1000 mg/day for 1–3 days) effectively terminated prolonged attacks or exacerbations with daily recurrences in 4 patients. In patients with severe nausea or vomiting, the route of administration of acute medication should be parenteral (i.e., by suppositories, nasal spray, or subcutaneous injection).
In many patients, episodes of VM are severe, long, and frequent enough to warrant prophylactic medication. Unfortunately, there is a lack of solid data derived from placebo-controlled trials. Thus far, there is only one randomized controlled trial of prophylactic treatment of VM, comparing the efficacy of flunarizine over 12 weeks to no prophylactic medical treatment. The frequency and severity of vertiginous episodes decreased with flunarizine, but the study can be criticized for lack of both blinding and application of placebo in the control group. Several retrospective and observational analyses have reported a reduction of intensity and frequency of attacks of VM with prophylactic migraine drugs such as metoprolol, propranolol, flunarizine, topiramate (just be aware of the rare angle closure glaucoma with this one: https://drcremers.com/2016/11/what-to-do-for-headaches.html, lamotrigine, valproate, and amitriptyline.  
One report notes carbonic anhydrase inhibitor acetazolamide, which is usually not used for migraine prophylaxis, helped (Baloh, 1996).
Note that VM symptoms can be variable and spontaneous remission is common. However, most experts agree that drugs that prevent VM symptoms are a good idea.  Talk to your MD about which medications to start with first:  In patients with hypertension a beta-blocker is usually the first option. For several drugs, such as flunarizine, valproate, and amitriptyline, weight gain can be a cause for concern. Sedation and other side-effects can be modified with slowly increasing the dose. Keep a diary & check in with your MD every 3months or so if you are doing well. Your goal is to decrease attacks to less than 60-70% of the time. 
In patients with constant dizziness, visual dependence, and unsteadiness in addition to episodes of VM, vestibular rehabilitation (this means doing exercises to move the little stones in the inner ear: I was very skeptical at first on this one as it looks a bit odd, but it cured my father in law faster than anything else) can be effective. Through this whole process you will likely be asked to see a psychiatrist. Do not fret, this happened to my esteemed Harvard colleague as well. It was sort of embarrassing for her but she offered it up and had a supernatural outlook. Take it in stride & see if there is anything they can help you with: though the best psychiatrists I have ever met, were strong in virtue, so find an honest and wise psychiatrist: they do exist.  One of my favorite psychiatrists at Harvard is Dr. Kevin Mayeres, he has a great website: http://www.purityispossible.com/; another is  Dr. Joanne Angelo, 403 Commonwealth Avenue, Boston, MA 02215, 617-266-3093

 2016;137:301-16. doi: 10.1016/B978-0-444-63437-5.00022-4.

Vestibular migraine.


During the last decades a new vestibular syndrome has emerged that is now termed vestibular migraine (VM). The main body of evidence for VM is provided by epidemiologic data demonstrating a strong association between migraine and vestibular symptoms. Today, VM is recognized as one of the most common causes of episodic vertigo. The clinical presentation of VM is heterogeneous in terms of vestibular symptoms, duration of episodes, and association with migrainous accompaniments. Similar to migraine, there is no clinical or laboratory confirmation for VM and the diagnosis relies on the history and the exclusion of other disorders. Recently, diagnostic criteria for VM have been elaborated jointly by the International Headache Society and the Bárány Society. Clinical examination of patients with acute VM has clarified that the vast majority of patients with VM suffer from central vestibular dysfunction. Findings in the interval may yield mild signs of damage to both the central vestibular and ocular motor system and to the inner ear. These interictal clinical signs are not specific to VM but can be also observed in migraineurs without a history of vestibular symptoms. How migraine affects the vestibular system is still a matter of speculation. In the absence of high-quality therapeutic trials, treatment is targeted at the underlying migraine.


dizziness; migraine; nystagmus; vertigo; vestibular

OK Journal:

 2016 Jul;21(4):51-4. doi: 10.1097/NRL.0000000000000076.

Establishing a “Vestibular Migraine Diagnosis Questionnaire” and Testing Its Validity.

Author information

  • 1Departments of *Neurology †Physical Medicine and Rehabilitation ‡Otorhinolaryngology, Head and Neck Surgery §Biostatistics and Medical Informatics, Ege University Medical School, İzmir, Turkey.



To establish a questionnaire and check its validity and reliability for the diagnosis of vestibular migraine in patients reporting recurrent vestibular symptoms.


Vestibular migraine is the most common cause for recurrent spontaneous vertigo. However, it is still underdiagnosed needing validated and reliable screening instruments such as ID Migraine, that can be used in primary care settings, dizziness, and migraineclinics.


Sixty consecutive patients referred to our dizziness clinic with recurring vestibular symptoms were given a questionnaire that they filled in, consisting of 8 short and simple questions. The questionnaire-based diagnosis was compared with the diagnosis based on face-to-face interview and clinical examination. Test stability was evaluated by asking the patients to fill in the questionnaire a week later during a second visit. κ analysis was used to assess item-specific test-retest reliability and also the conformity between the questionnaire-based diagnosis and the clinical diagnosis.


The conformity between the clinical diagnosis and the diagnosis based on the questionnaire was 83.3% and the κ coefficient was 0.666 (good). Sensitivity of the questionnaire was 82.8% (24/29) and the specificity was 83.9% (26/31). The κ values in test-retest repetition were good to excellent (0.71 to 0.87) when each question was considered.


The validity of the “Vestibular Migraine Diagnosis Questionnaire” was good and its reliability was good to excellent indicating that it can be used as a screening tool in identifying patients with vestibular migraine in our country.

More clues but in Forgein Journals:

 2016 Jun 2. pii: S1808-8694(16)30103-3. doi: 10.1016/j.bjorl.2016.04.022. [Epub ahead of print]

Prophylactic treatment of vestibular migraine.

Author information

  • 1Departamento de Otorrinolaringologia e Cirurgia de Cabeça e Pescoço, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP, Brazil. Electronic address: marciosalmito@yahoo.com.
  • 2Departamento de Otorrinolaringologia e Cirurgia de Cabeça e Pescoço, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP, Brazil.



Vestibular migraine (VM) is now accepted as a common cause of episodic vertigo. Treatment of VM involves two situations: the vestibular symptom attacks and the period between attacks. For the latter, some prophylaxis methods can be used. The current recommendation is to use the same prophylactic drugs used for migraines, including β-blockers, antidepressants and anticonvulsants. The recent diagnostic definition of vestibular migraine makes the number of studies on its treatment scarce.


To evaluate the efficacy of prophylactic treatment used in patients from a VM outpatient clinic.


Review of medical records from patients with VM according to the criteria of the Bárány Society/International Headache Society of 2012 criteria. The drugs used in the treatment and treatment response obtained through the visual analog scale (VAS) for dizziness and headache were assessed. The pre and post-treatment VAS scores were compared (the improvement was evaluated together and individually, per drug used). Associations with clinical subgroups of patients were also assessed.


Of the 88 assessed records, 47 were eligible. We included patients that met the diagnostic criteria for VM and excluded those whose medical records were illegible and those of patients with other disorders causing dizziness and/or headache that did not meet the 2012 criteria for VM. 80.9% of the patients showed improvement with prophylaxis (p<0.001). Amitriptyline, Flunarizine, Propranolol and Topiramate improved vestibular symptoms (p<0.001) and headache (p<0.015). The four drugs were effective in a statistically significant manner. There was a positive statistical association between the time of vestibular symptoms and clinical improvement. There was no additional benefit in hypertensive patients who used antihypertensive drugs as prophylaxis or depressed patients who used antidepressants in relation to other prophylactic drugs. Drug association did not show statistically significant results in relation to the use of a single drug.


Prophylactic medications used to treat VM improve the symptoms of this disease, but there is no statistically significant difference between the responses of prophylactic drugs. The time of vestibular symptom seems to increase the benefit with prophylactic treatment.

[Clinical characteristics of 100 vestibular migraine cases].

[Article in Chinese]



To analyze the characteristics of vestibular migraine (VM), in order to understand the auditory and vestibular function.


One hundred cases of confirmed or suspected VM patients were observed. Routine examination including pure tone test, vestibular dual temperature test and vestibular evoked myogenic potential(VEMP) and video head impulse test(v-HIT) Were conducted.


The incidence of male and female was about 1.00 : 2. 57. The average age of onset was 47 years, of which the youngest was 19 years old, and the oldest was 74 years old. Ninty-three cases of patients presented with vestibular sensitive performance, including photophobia, phonophobia,or motion sensitive. Fourty-two patients had migraine at the onset of the disease. Thirty-four patients had cochiear symptoms, including tinnitus, ear fullness, or epicophosis. In seventeen cases of fatigue, tension or poor sleep can cause vertigo. Nine patients had low blood pressure, 7 patients presented with hypertension. Two cases of vertigo were closely related to the change of position, and 1 case had visual aura. In the experiment, 94 patients had undergone VEMP test,with 44 cases of abnormal VEMP value. Seventy-nine patients had been examined v-HIT,of whom 2 patients were abnormal (both of which were reduced). Pure tone audiometry was abnormal in 35 cases. Five cases of patients showed abnormal vestibular-double temperature test.


Vestibular migraine is more prone to female, with young middle age, and can be accompanied by cochlear symptoms. Vestibular function tests (low frequency and high frequency) are normal.

 2016 Nov;64(11):790-796.

[Dehiscence syndromes : Diagnosis and treatment].

[Article in German]



Dehiscence syndromes of the semicircular canals are a relatively new group of neurotological disorders. They have a variety of symptoms with hearing/balance involvement. Younger patients have clinically relevant symptoms in only about one third of cases. In addition to etiology and pathogenesis, the present paper describes diagnostic and therapeutic possibilities using a patient series of the authors.


This nonrandomized prospective study included 52 patients with uni-/bilateral dehiscence syndromes of the superior and/or posterior canal (SCDS/PCDS), diagnosed with high-resolution computed tomography (HR-CT) of the petrous bone. Of 41 patients undergoing surgical therapy for severe symptoms-predominantly vertigo attacks (Meniere-like) and/or falls (Tumarkin crises)-31 received single-sided hearing implants.


Of the 41 patients with transmastoid superior and/or posterior canal occlusion, 30 showed a significant improvement of balance in the Dizziness Handicap Inventory (DHI); the dizzy spells ceased. A positive outcome was correlated with the severity of the preoperative disorder; a poor outcome (nonsignificant increase in DHI, recurrent vertigo of various qualities/frequencies) with the comorbidities vestibular migraine, Menière’s disease of the contralateral ear, and a dehiscence size exceeding 4 mm.


The more severe the vestibular symptoms, the better the outcome of surgical therapy. Auditory symptoms (nonspecific aural fullness, hyperacusis) do not generally respond well to surgical therapy. Cochlear implants have an additional beneficial effect; comorbidities should be considered as (relative) contraindications.


Cochlear implants; Hearing loss; Menière’s disease; Tinnitus; Vertigo
Mar 2008

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Mar 2008

Mar 2008

This is a little letter I wrote to some friends and acquaintances tonight.
“Since 1861, no doctor has been able to trace the exact cause or cure of Meniere’s Disease. As most of you know, I have a so called double whammy diagnosis of Migraine Associated Vertigo and Meniere’s Disease. I’ve tried just about all of the conventional and unconventional treatments to put it—or them—at bay. I’ve improved, but medically speaking, I’ll probably never be completely cured.
Over the last 3 years, after firing several doctors, two “good” docs have told me I have Meniere’s. They said it’s severe and atypical, which isn’t a good thing.
Another doctor, my best doc thus far, told me I have both Migraine Associated Vertigo (MAV) and Meniere’s. Recently, he added some complexity by telling me I might have a perilymph fistula (PLF), which is a small tear or rupture in the inner ear that can wreak all sorts of havoc, and can actually create a cerebral spinal fluid leak. If I have a fistula, it can be repaired surgically, but then again, it can re-open. Moreover, there have been several cases where patients actually have all three ailments: Meniere’s, MAV, and PLF.
Lots of fun if you like being dizzy and disoriented.
There’s all sorts of theories—none completely proven—as to why people acquire these ailments. They also have one thing in common: No real, true silver bullet test to confirm that’s exactly what the patient has. Great if you’re a clinical, scientific-type curious about elusive, incurable afflictions, but not so good if you’re a patient who just wants a good ol’ fashioned straight answer or cure.
Some say Meniere’s and MAV may be caused by an autoimmune virus. I probably had that back in 2005 when I was in the hospital a whole bunch of times after being enviably healthy for most of my life….but the docs couldn’t figure it out. It could be caused by multiple/chronic ear infections, ultimately causing intractable damage to the inner ear. Had that, too. Might be some distant ramification of Lyme Disease. One health practitioner—a good one—thought I’d had it in the past, but docs gave me the wrong blood test. Could be caused by head trauma. I’ve had 3 concussions. Could be caused by an upper respiratory tract infection. Had that real bad in 2005. Might be barometric pressure issues. Weather is definitely a trigger. Some foods can put me under, but docs say I’m not allergic to anything but dust. Cincinnati is #1 in the nation for migraines, so I guess that’s somewhat of a hint for me, but I don’t exhibit all of the classic symptoms of MAV….or for that matter….Meniere’s…..or PLF. It’s a combination of a bunch of things. Some say Meniere’s is caused by too much salt. A little bit of correlation there, but not real, hard, true causation after experimenting on myself. Some say stress….maybe a little bit of that, but not too much. Some say ischemia…..nothing at all like that. Too much caffeine. Never was a big coffee drinker. Too much alcohol. Never was a big drinker.
In line with geopolitical issues with America’s most potent competitor, maybe it’s all part of a vast Chinese conspiracy. No…not cheap, lead paint-laden toys. MSG in Chinese food kills me.
After all of the tests, constant study, interaction with fellow patients, and all sorts of fascinating and sometimes meaningless conversations with doctors over the last 3 years, I’ve finally have a good idea as to what caused all of this:
Yes. It’s quite simple. Since 1994, my bosses—mostly MBAs from a far distant palace of intriguing balance sheets and interesting ways of interpreting taxation and compensation— always seemed to always be putting me into the weirdest, whackiest, craziest situations. Some of it was indeed fun and adventurous, but some of it was….well……just a little bit crazy when I look back at it.
Always having to turn around some troubled account. It usually went something like this from a boss who just bought some real expensive new toy or a big house he didn’t really need. “Listen, if you can’t take this account in San Francisco and turn it around, we might lose the whole $30 million account across the country.”
Managers kept quitting…..mostly for the right reasons. The problem….predictably…. was simple: The contract was just bad.
Got it turned around after fixing some simple things and getting some price increases. A few good truck drivers actually educated me on that during my first two weeks on the job.
That was it.
Always having to fly somewhere to fix something after getting a real complex financial spreadsheet from some guy at corporate HQ who never visited the account.
Always being put in charge of the most difficult—and sometimes borderline narcissistic and psychotic—customer who never seemed to understand that $1 million in cost savings is roughly equivalent to $10 million in sales, and that return on equity—not his bonus based on sales quotas or exploiting the tax code—was the ultimate measure of business success.
Always having to “re-engineer” some account with well paid, but curiously militant employees whose collective goal in life was to do the exact opposite of John F. Kennedy’s famous speech in the early 1960s.
Interestingly, with many of these accounts, I always seemed to have some underperforming vendor who wanted to give me tickets to the next big game, but wanted a price increase at the same time. Another vendor—often saddled with all sorts of debt—- wanted me to experiment with his latest breakthrough in their technology, but always seemed to fail to mention that beta tests always have too many bugs to be properly functional & provide a real return on investment.
Uh oh….I’m starting to sound too much like whining Woody Allen.
Let me put it in more proper, sensible perspective.
As Ross Perot once said about management: “The principles of leadership are timeless because in a rapidly changing world human nature remains constant.”
Folks just want something for nothing.
It was kind of like being involved in some bizarre, morphed, amalgamated version of Seinfeld, The Office, Office Space or Curb Your Enthusiasm.
A comedy of errors that should’ve never happened in the first place.
So, in sum, it’s basic and simple…..just as most things really are. After all, the elite power players in our society —-lawyers, doctors, politicians, and corporate executives—- always seem to try to make things more complex and mysterious than they really are.
In this case, as far as my three year odyssey with the medical establishment goes—-it has nothing to do with some sort of exotic etiological agent….no elaborate epidemiological study will explain this. In the case of these diseases, new medical technology or advances in biophysics or medical physics only seem to add unnecessary complexity to the fray instead of narrowing it down to what everyone really wants: A Real Cause & Real Cure.
“Progress”, after all, especially in the early 21st century, is often an oxymoron.
I do have some proof of this. Patients have a gut instinct about what caused their ailment, and doctors continue to argue amongst themselves without listening…..and curing.
Below is the best explanation I’ve ever read. It’s from the blog of a Meniere’s patient, and lends credence to what I’ve noted above. I got a kick out of this, and strongly believe it’s at least partially true based on my experiences.
It explains a lot about the disease, and the contemporary world of business.
In the end, the counterintuitive nature of the world has just made me plain old dizzy.
Enjoy. “
The 10/20/30 Rule of PowerPoint
by Guy Kawasaki

(Link to Kawasaki’s Biography: en.wikipedia.org/wiki/Guy_Kawasaki)
I suffer from something called Ménière’s disease—don’t worry, you cannot get it from reading my blog. The symptoms of Ménière’s include hearing loss, tinnitus (a constant ringing sound), and vertigo. There are many medical theories about its cause: too much salt, caffeine, or alcohol in one’s diet, too much stress, and allergies. Thus, I’ve worked to limit control all these factors.
However, I have another theory. As a venture capitalist, I have to listen to hundreds of entrepreneurs pitch their companies. Most of these pitches are crap: sixty slides about a “patent pending,” “first mover advantage,” “all we have to do is get 1% of the people in China to buy our product” startup. These pitches are so lousy that I’m losing my hearing, there’s a constant ringing in my ear, and every once in while the world starts spinning.
Before there is an epidemic of Ménière’s in the venture capital community, I am trying to evangelize the 10/20/30 Rule of PowerPoint. It’s quite simple: a PowerPoint presentation should have ten slides, last no more than twenty minutes, and contain no font smaller than thirty points. While I’m in the venture capital business, this rule is applicable for any presentation to reach agreement: for example, raising capital, making a sale, forming a partnership, etc.
Ten is the optimal number of slides in a PowerPoint presentation because a normal human being cannot comprehend more than ten concepts in a meeting—and venture capitalists are very normal. (The only difference between you and venture capitalist is that he is getting paid to gamble with someone else’s money). If you must use more than ten slides to explain your business, you probably don’t have a business. The ten topics that a venture capitalist cares about are:
Your solution
Business model
Underlying magic/technology
Marketing and sales
Projections and milestones
Status and timeline
Summary and call to action

You should give your ten slides in twenty minutes. Sure, you have an hour time slot, but you’re using a Windows laptop, so it will take forty minutes to make it work with the projector. Even if setup goes perfectly, people will arrive late and have to leave early. In a perfect world, you give your pitch in twenty minutes, and you have forty minutes left for discussion.
The majority of the presentations that I see have text in a ten point font. As much text as possible is jammed into the slide, and then the presenter reads it. However, as soon as the audience figures out that you’re reading the text, it reads ahead of you because it can read faster than you can speak. The result is that you and the audience are out of synch.
The reason people use a small font is twofold: first, that they don’t know their material well enough; second, they think that more text is more convincing. Total bozosity. Force yourself to use no font smaller than thirty points. I guarantee it will make your presentations better because it requires you to find the most salient points and to know how to explain them well. If “thirty points,” is too dogmatic, the I offer you an algorithm: find out the age of the oldest person in your audience and divide it by two. That’s your optimal font size.
So please observe the 10/20/30 Rule of PowerPoint. If nothing else, the next time someone in your audience complains of hearing loss, ringing, or vertigo, you’ll know what caused the problem. One last thing: to learn more about the zen of great presentations, check out a site called Presentation Zen by my buddy Garr Reynolds.
Written at Atherton, California
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