You can find the answers to your questions from this site. mddsfoundation.org/
Dr Ch is a physician‐scientist in the Department of Neurology at the University of
California at Los Angeles (UCLA)the head of the new MDds research study, for the next 3 years.
Dr. Yooni Cha replies to the top 10 questions
The questions are:
1. There are different ideas of what is causing MdDS, including the “internal-model theory”, and
also that there’s a migraine-connection, utricle dysfunction etc. Do you feel that any given theory
gives an entirely satisfactory explanation and if so why?
***MdDS is a disorder of neuroplasticity. MdDS behaves like other disorders of maladaptive
cortical plasticity, like refractory depression, chronic pain, post traumatic stress disorder, and
tinnitus. These syndromes are all triggered by an initial stimulus that may be peripheral and
episodic, but they somehow become primary central disorders. These disorders have remissions
and unexplained recurrences because the brain retains a memory for the initial conditions that
created the perception of the symptoms. For example, tinnitus may start as an inner ear disorder
associated with sensorineural hearing loss, but functional brain imaging studies show that the
primary or secondary auditory cortex is hyperactive in these patients. The question is whether
there is some predisposition to this process or whether one just happens to be unlucky in being
exposed to the perfect conditions that allow this hypersensitization to occur.
I can’t see any reason why MdDS would be associated with actual damage to the inner ear. The
utriclar dysfunction theory has been proprosed but there is just no mechanism for utricular
dysfunction during the exposures that lead to MdDS. I can see how some damage to the inner
can cause rocking sensations, but there doesn’t seem to be any evidence that true damage to the
inner ear occurs in this disorder. One may argue that there is abnormal brainstem processing of
utricular function but this would be theoretical only.
There is a connection with migraine, but this is mainly with the spontaneous appearance of
chronic rocking dizziness in young patients with a history of migraine headaches (particularly
with aura) or in the re-emergence of the MdDS-like symptoms after the initial motion triggered
MdDS has passed. This is not surprising since patients with migraine tend to have other kinds of
spontaneous perceptual problems such as the aura, motion sickness, panic disorder, etc.
2. It seems MdDs can be retriggered without another motion-experience being present;
perhaps from a bad migraine or the flu etc. If you as a physician agree with this, would this point
to that there might be the same mechanisms going on for typical post-cruise MdDs, and for
people who exhibit the same symptoms without there being a motion-trigger present; especially
given that they too experience the universal sense of feeling better in passive motion?
***From my experience, the people who get this spontaneously behave a little differently than
the true motion-triggered MdDS patients. They seem to be younger, are much more likely to
have migraine headaches, and they don’t seem to consistently feel better with motion. Some
people feel much more motion sick with motion, which never seems to happen with true MdDS.
Patients with migraine are prone to experiencing all kinds of other spontaneous symptoms
related to motion. They are much more likely to motion sick and to be sensitive to visual motion.
There is evidence from transcranial magnetic stimulation studies that their brains are somewhat
hyperactive. That being said, the mechanism for why the symptoms start spontaneously would
have to be different between these spontaneous events and motion triggered MdDS, BUT, the
areas of the brain that are affected could still be the same.
3. Motion being the trigger, why do you think it is that it can take anything from a few hours
up to a few days before the symptoms start; this as opposed to them always starting immediately
upon cessation of motion-stimuli?
*Interesting question since some people do experience the symptoms right away. Often times,
patients who are getting MdDS after a cruise are almost immediately getting into another
vehicle, like a car or plane. I’m not entirely sure why the delay is there but if there is some kind
of “feed-forward” mechanism that is triggered in the brain by the motion exposure, then it may
take some time for these connections to become strong enough to start creating conscious
4. Do you consider medication such as benzodiazepines to be helpful, neutral or perhaps even harmful
in the goal towards having complete resolution of symptoms; especially in the earlier stages of mdds?
***There is no way to know if they are harmful in the longrun except to randomize dozens of
patients with MdDS to either the medication or placebo and do a prospective study. In general, if
the patient can get by without it, then I let them try. I am also careful about dose escalation
because of tolerance and dependency but this hasn’t been a problem, interestingly.
I usually use a small dose of clonazepam (a long-acting benzodiazepine) for severe symptoms. I
never use alprazolam (xanax) because it has too many problems with addiction and dose
escalation because of its short half-life.
5. Some doctors promote taking medication prior to further travel (regardless if the patient is in
remission or not), what’s your take on this? If you support medication, what have you found to
***I tell patients who are prone to developing MdDS (since many have recurrent episodes) to try
to get a lot of rest during their trips. Sometimes this requires taking a sleeping aide or a
benzodiazepine. Generally something shorter acting like Ativan or Valium would work, since the
person has to be able to wake up at the other end of the flight. This is only a significant issue
with flying, since people have to fly. Since patients generally don’t HAVE to take cruises or go
on road trips and I don’t have many suggestions for them, except to get plenty of rest during and
after the trip. Taking something sedating prior to the actual flight is probably not practical, unless
someone is with the patient to take care of all of the travelling arrangements.
6. A few members of our support group seem to only have this every other day (after perhaps years of every day symptoms). While it isn’t uncommon for this to happen for a little while as symptoms resolve entirely (or so I’ve read), for these people it seems they’re stuck in some kind of perpetual loop, now having it every other days for years. How could this be? Is there any good analogy with other diseases/things here?
***I don’t know why this happens, since the pattern is not consistent from person to person. But,
we have to be aware that the state of the brain is never the same from minute to minute and
definitely not from day to day. This is influenced by all kinds of stimuli from the amount and
quality of sleep obtained the night before, what is eaten, the ambient temperature, whether you’ve
just argued with your spouse, where you are in your menstrual cycle, what you’re thinking about,
etc. along with how much motion exposure is received each day.
7. Some think that there is a connection between mdds and migraines, and it does seem like migraines are more common among mdds-sufferers than the general population. This could of course be explained by simple correlation and not causation, or maybe that mdds is causing migraines and not vice versa. So is there any real connection?
***I see the connection being with MdDS sufferers who tend to get recurrent episodes and with
people who develop spontaneous onset of rocking symptoms. Some patients have also indicated
that they developed headaches or had a recurrence of their migraine headaches when their MdDS
symptoms started. But, I don’t see a much greater incidence of migraine in MdDS patients who
present with very typical cases. Migraine clearly does not explain the majority of typical MdDS
8. In your opinion, could MdDs have anything to do with neck-problems (cervical vertigo)?
*That’s very unlikely.
9. In your opinion, could MdDs be related to – or in fact be - Microvascular Compression?
***This is almost impossible. People who espouse this theory have to explain why getting on a
boat would make an artery and a nerve in the brainstem suddenly become closer to each other.
10. what is the relationship between MdDs and anxiety, if any?
***The symptoms of MdDS are clearly anxiety provoking. Some degree of this is in dealing
with an unresponsive medical system that does not validate your (the patient’s) symptoms. Some
of this is in not knowing if the disorder will ever stop. Some of this is because your normal social
support group falls apart when you can’t engage in normal relationships anymore.
However, I think that some degree of this might actually be part of the disorder itself. I’ve
noticed that people who have had MdDS for a long time will start to have a “spread” of
symptoms. They might become tremulous, get anxious, develop tinnitus, get headaches, etc. It
would be interesting to study whether MdDS sufferers had suffered from anxiety and depression
prior to the onset of MdDS. This would be very interesting in terms of coming up with a model
for why certain people get persistent disorders like this. This study would be hard to do in
retrospect because patients tend to overestimate how healthy they were before the onset of a
And if you have the time:
11. Where do you see the knowledge about this condition, as well as treatment-options,
going in a decade from now?
The next phase in understanding this disorder is with functional neuroimaging. We need to be
able to see how the brains of MdDS patients functions differently, processes information
differently, or has different baseline activity than asymptomatic people. My plan is to introduce
repetitive transcranial magnetic stimulation as a treatment option based on these functional
imaging differences. This modality has been approved for the treatment of refractory depression
and there are many positive clinical trials in its use for chronic pain and tinnitus. It has even been
used to improve ambulation in parkinson’s disease and can modify many movement disorders.
The challenge in MdDS is to find the right target and the right settings so there will need to be
many iterations of a treatment paradigm to get it right, but I don’t believe that more oral
medications will be the way to go.