Timothy C. Hain, MD Page last modified: November 11, 2017
Mal de Debarquement or "MdDS" (or MDDS) is a type of vertigo and imbalance that occurs after getting off of a boat. The usual situation is that of a middle aged woman who has gone on a cruise. We use the abbreviation "MdDS" because it is currently favored over the simpler MDD. It has been pointed out that "MDD" can be confused with other disorders. MdDS has attracted more interest recently, and there are several recent reviews -- including Van Ombergen et al (2015), and Hain and Cherchi (2016).
To our knowledge, the first reference to the syndrome was made by Erasmus Darwin, in 1796. He wrote:
"Those, who have been upon the water in a boat or ship so long, that they have acquired the necessary habits of motion upon that unstable element, at their return on land frequently think in their reveries, or between sleeping and waking, that they observe the room, they sit in, or some of its furniture, to librate like the motion of the vessel. This I have experienced myself, and have been told, that after long voyages, it is some time before these ideas entirely vanish. The same is observable in a less degree after having travelled some days in a stage coach, and particularly when we lie down in bed, and compose ourselves to sleep; in this case it is observable, that the rattling noise of the coach, as well as the undulatory motion, haunts us. " (Darwin, 1796).
A 50-year-old woman went on her first ocean cruise. She had some motion sickness on the cruise, which responded to transdermal scopolamine. Immediately after returning from the cruise and getting onto solid ground, she developed imbalance and a rocking sensation, accompanied by fatigue and difficulty concentrating. This persisted for months. She felt better however when she was driving. Her description was “Imagine feeling like you are on rough seas 24 hours a day, 7 days a week.”
A related case ? An avid cross country skier noted that after she would come home from a day of skiing, she developed a sensation as if she was still skiing until she went to sleep. She was always fine in the morning. Many patients with MdDS or rocking symptoms say they have "motion memory" meaning that they feel as if they are moving after driving, or sometimes even just riding on an elevator.
Table1: Characteristics of MdDS
Median Duration (mo)
Cha et al, 2008
Hain et al, 1999
3.5 years (6 mo to 10 years)
Brown and Baloh, 1987
Total or (average)
months to years
Table 1 summarizes the available literature about MdDS. Ombergen et al (2015) in a review, discovered far more patients than this, and the interested reader is referred to their paper. Also, Dai et al (2017) reported in a single study, about 120 patients.
MdDS is a disorder that mainly affects women (85%) in their mid 40's. Except in California where a larger number of men are affected, (the site of Dr. Cha's study), almost all individuals with MdDS are women. They typically have gone on a 7-day cruise. After getting off the boat, or "debarking" (debarquement), they immediately develop a rocking sensation, as if they are still on the boat.
Here we define MdDS as rocking lasting for at least a month. This leaves the land-sickness group out. This definition was also used by the majority of studies reviewed by Ombergen et al (2015).
|Age of onset of patients in Chicago Dizziness and Hearing database, as of 2015.|
The graph above is drawn on a much larger and more representative sample of patients than from our study of 1999, again mainly women (153/181 -- 85%), it shows that the distribution mainly includes females between the ages of 30-60. Although females predominate, for the treatment study of Dai et al (2017), positive effects of treatment were similar among genders.
Most patients with MdDS get better when they drive a motor vehicle. Some also are better when they are simply a passenger. This varies from the situation with Migraine patients or Meniere's patients, who generally get worse (Sharon and Hullar, 2014). This feature has not been incorporated into the definition of MdDS, but it would seem a reasonable addition.
Dai et al (2017) reported that their MdDS patients most commonly complained of rocking, swaying, bobbing, "gravity pulliing", and "trampoline walking". They had a sway frequency that was predominantly 0.2 Hz. This is very slow -- with a full cycle occuring over about 5 seconds.
Dai et al (2017) also noted that recurrent MdDS was reported by 23% of their 120 patients treated with "classic" MdDS.
As of 2015, we had encountered 181 MdDS patients in our dizzy clinic database out of an "n" of about 18,000 patients with assigned diagnoses. This suggests that only roughly 1/100 dizzy patients have MdDS. As about 5% of the population develops "vestibular" dizziness per year, if we assume that our clinic sees MdDS as a representative proportion of all dizzy patients, a very very rough estimate as to the prevalence of MdDS is 0.05% (this is the same as 0.5/1000 persons). Or to put this into real-world terms, assuming 300 million persons in the United States, a 0.5 persons/1000 people prevalence works out to a total of 150,000 persons with MdDS in the US. Compared to land sickness (which happens in roughly 50% of persons who go on boats), this is an unusual condition, and far less common than other dizzy conditions, say vestibular migraine (1% of population -- 3 million) or Meniere's disease (2/1000 people, 600,000 total in US or 0.2%). Note that this estimate could easily be wrong (probably too much) by an order of magnitude.
The figure above, from our 1999 paper, illustrates "worst case" durations -- it does not reflect the usual duration of symptoms. This is because the study group from our 1999 paper were persons with very severe MdDS. A prospective study would be needed to answer this question properly.
Table 2: Features Distinguishing MdDS from Land-sickness (LDS)
1 or more months
2 days maximum
About 90% female
Motion-sick on boat
Relieved by driving
There are several variants of motion induced sickness that are not MdDS. Table 2 lists the features that distinguish MdDS from simple land-sickness. Land-sickness (LDS) is common, and between 41% and 73% of persons disembarking from seagoing voyages experience a brief unsteadiness syndrome (Gordon, Spitzer et al. 1995; Cohen 1996; Gordon, Shupak et al. 2000). Common LDS typically persists for 2 days or less. Persons with LDS are also likely to have sea-sickness, (Gordon, Spitzer et al. 1995) while persons with MdDS generally are untroubled by sea-sickness. Males and females do not appear differ significantly in the incidence, intensity, or duration of land-sickness symptoms. (Cohen 1996). LDS, confusingly, is also termed "mal de debarquement" by some. Table 1 does not include reports or data concerning subjects who symptoms that last less than 1 month, i.e. potential land-sickness, except for the work of Cha, in whom the duration of patients with "classic" MdDS could not be determined due to study design(Cha, Brodsky et al. 2008). Dai et al (2017) also distinguish between "sea legs", and "MdDS".
Ombergen, Rompaey, Maes, Heyning and Wuyts (2015), in a "systemic review", invented another nomenclature -- transient "MdD" symptoms < 48h, persistent MdDS (> 3 days to several years). "Transient MdD", using their nomenclature is equivalent to land-sickness as defined above. There is an undefined group for Ombergen et al (between 2-3 days). From 3 days to several years would be MdDS as we define here, and then from "several years" onward, no name.
MdDS also has some similarities to motion sickness (sea sickness, mal de mer). However, MdDS is again easily distinguished by the shorter duration of motion sickness and gender distribution. Persons with MdDS reliably have relief of symptoms when in motion, such as driving a car, but experience recurrence of rocking once motion has stopped (Hain, Hanna et al. 1999; Cha, Brodsky et al. 2008). In motion sickness, many persons find driving very difficult. This is also often true for persons with vestibular disorders and migraine (Sharon and Hullar, 2014).
MdDS also overlaps with a little studied group of patients called "rockers", who develop similar symptoms to MdDS, without a preceding motion exposure. (Cha 2012) Another name for the same group is "non motion triggered MdDS" -- which is of course a contradiction in terms, but it presumably serves to widen the spectrum of "MdDS". Another term is "spontaneous MdDs" (Dai et al, 2017), again an odd term as there was no "Debarquement". Often these patients develop head or trunk rocking, which is called "titubation". In our clinical experience, the age, gender and pattern of medication responsiveness of this group are similar to those of MdDS. Although titubation is associated with cerebellar disturbance, evidence of cerebellar damage is generally not found in "rockers". Cohen et al (2015) stated that their term for "rockers" is "spontaneous MdDS ". They found that these people were more difficult to treat with habituation but still "the cure rate was more than 50%".
We have also encountered a few "rockers", who developed this symptom after a well defined CNS lesion, generally a small stroke. This is usually in the motion processing area of the brain.
It is the general opinion that MdDS is generally not caused by an injury to the ear or brain. At this writing (2016), the predominant opinion is that MdDS is a variant motion sickness. While this doesn't explain why MdDS seems to mainly affect women in their 40-60's it does seem to account for observations of naval personnel who have a similar land-sickness experience.
Some dizziness experts believe that MdDS is caused by a variant of migraine. We do think that migraine increases risk of MdDS. We have seen many patients who developed MdDS when exposed to motion around the time of their period (which is also a high risk time for migraine). This might explain why some cruises are tolerated without distress, and others not.
Other theories about the cause of MdDS it that is caused by inappropriately high weighting of somatosensory input for balance (Naichem et al, 2004). As somatosensory information and vestibular information are both unreliable on a boat, this is a difficult explanation to follow. We think that the internal model theory explanation (which follows) is the better one at this writing (2014).
A recent conjecture is that MdDS is caused by adaptation to roll while rotating. In other words, if one is rocking side-side (roll), and also rotating the head, for long periods of time, one might develop an inappropriate cross-coupling between roll and rotation (Dai et al, 2009; 2014). Our position on this idea is that it could explain brief (2 hour) symptoms after getting off of a boat, and also offers an explicit hypothesis that might be tested formally (i.e. people who do a lot of head rotation on a boat would be more likely to get this than people who sit quietly). However, overall we are dubious that this conjecture is correct. Why would women mainly develop inappropriate cross-coupling ? Why wouldn't people get rid of this by simply walking around with their eyes open ?
Dai et al (2017) wrote "we postulate that the neurons on both sides of the brainstem oscillate with the activity flowing back and forth, at about 0.2 Hz to activate the body and legs into rocking and swaying at 0.2 Hz. The source of the 0.2 Hz drive is unknown, but it is likely to originate in the nodulus of the vestibulocerebellum, which exerts control over the velocity storage system (42–47). Such activity, which has been found in the cerebellar cortex of the nodulus in the rabbit (48), can be brief or can last for years. " We are not entirely sure what to make of this conjecture, as we would not know how to confirm or deny its veracity.
Because MdDS largely occurs in females, it may also have something to do with sex hormones, such as estrogen or progesterone. In fact, we have noted a pattern that if one asks, it is often the case that the woman who develops MdDS was having a period while on the boat. MdDS could also be genetic, related to two copies of the 'X' chromosome perhaps combined with other susceptibility factors. The "Norwalk" virus is common on cruise ships, and perhaps this syndrome is somehow related to this virus.
It seems unlikely to be a psychological disturbance -- although it is always difficult to entirely exclude psychological problems, the male:female ratio and other aspects of this disorder would make this unlikely.
Moeller and Lempert (2007) recently suggested that MdDS is due to "deafferentation" or panic. We disagree with both of these ideas.
Cha et al (2012) reported changes in brain connectivity in persons with MdDS. This study, however, was done in a powerful MRI scanner, which can cause temporary dizziness by itself. MdDS seems to be associated with changes metabolism in the brain, in circuits related to vision, vestibular processing and emotional reactions. It would be interesting to see how much of this is due to MdDS and how much is secondary to being dizzy. In 2015, in a study published in PLOS-1 (open-access), Cha and Chakrapani reported that " Individuals with MdDS show brain volume differences from healthy controls as well as duration of illness dependent volume changes in (a) visual-vestibular processing areas (IPL, SPL, V3, V5/MT), (b) default mode network structures (cerebellar IX, IPL, ACC), (c) salience network structures (ACC and IFG/AI) (d) somatosensory network structures (postcentral gyrus, MCC, anterior cerebellum, cerebellar lobule VIII), and (e) a structure within the central executive network (DLPFC). " 80% of the 29 subjects in this study were female, almost all were middle aged, and almost all had symptoms for more than 1 month; thus they met the conventional criteria for this MdDS. The authors themselves point out that the brain volume differences might be due to compensatory processes rather than causes of symptoms. They also note that the results were presented with "uncorrected p-values and it can be argued that many of the voxels seen in the contrasts could be seen by chance". Overall, these studies do not seem to have added much to our understanding of MdDS.
There are some reports of MdDS following use or withdrawal from serotonergic medications. The connection here is that serotonin may inhibit glutamate, an excitatory transmitter in the vestibular nucleus (Smith and Darlington, 2010.). This idea also provides an explanation why serotonergic medications may help MdDS (see treatment section).
Note that the MdDS of "Mal de Debarquement" has nothing to do with the other MdDS of "Manic Depressive Disorder". The support group for MdDS, being sensitive to this, has suggested that the proper name of the syndrome would best be "MdDS ". Our own feeling is that there are many medical disorders that share initials with other disorders (PAN is an example -- periodic alcohol nystagmus and periodic alternating nystagmus), and one should not get too anxious about the initials
A plausible mechanism for the development of MdDS is that it is due to formation of an inappropriate internal predictive model. We first proposed this idea in 2007 (Hain and Helminski, 2007). Internal models are sophisticated estimators that have been used to explain such difficult observations that one cannot "tickle" oneself (see the work of Wolpert (1995) and others). Examples of internal models are very easy to find in daily life -- suppose you pick up a suitcase, expecting it to be full, but it is empty ! Internal models are sophisticated methods of dealing with events even before they happen ! (Blakemore, 1998)
On a boat, one is faced with a difficult balancing problem, with components of rotation (pitch plane rotation -- about the axis between the ears), and linear movement (surge -- front-back movement of the boat). Both are somewhat predictable as the boat is large and it's interface between it and the ocean constrains it to low frequencies of movement.
Lets take an example -- when the boat pitches (rotates) forward, there is a small amount of pushing the person backward accompanied by a tilt of the visual world as the angle between upright and the boat surface becomes more acute. To stay upright in response to pitch, a person should not activate their ankle muscles much as inertia tends to keep their body upright. Vision is accurate on the deck but inaccurate inside. Thus vision is unreliable. Although there is rotation around the ankle joint, and thus somatosensory input, there should be no "righting" response from the person because the body is upright in space. Visual responses are correct on deck and incorrect inside, and thus a "rule" cannot be made. The rule then for pitch rotation of the boat, one should ignore somatosensory information signaling rotation . Thus for pitch of the boat, a selective "downweighting" of somatosensory information, or both somatosensory and visual information according to context, would be a reasonable adaptation (or rule).
For linear acceleration of the boat under the person, or "surge" as it is called in nautical contexts, inertia attempts to keep the person still in space, but due to shear force at the feet, the person becomes destabilized and rotates at the ankles. Then vision, vestibular and somatosensation senses are activated by the bodily rotation with respect to the boat, and an active response is needed to prevent a fall. Thus for surge of the boat, no relative sensory reweighting would be needed, although increased responses to all types of input might be helpful.
How does the brain figure out which rule to apply ? We propose that people develop a predictive model of the boat motion, and use their prediction to select the rule to apply for boat motion (and avoid falling). Supporting this general supposition, Denise and Darlot (1993) suggested that the cerebellum was a predictor of neural responses, and implemented an internal model, that might be relevant to motion sickness.
Normally, it seems likely that over a few days, people develop an internal model of periodic motion on the boat so that they predict and cancel out input (visual or somatosensory) that is phase-locked to pitch rotation, and enhance responses due to surge that is not. The internal model normally is disposed of once the person returns to terra firma, again over a period of hours to days. Persons with MdDS are unable to dispose of this internal model, which is only useful when they are exposed to periodic motion (such as when driving a car).
We have encountered a few patients whose motion after-effects are specific to motion - -when they cross country ski, they have a motion after-effect of skiing, etc. Of course, this has to be an internal model problem.
The internal model theory explains most of the features of MdDS.
What does the data say about mechanism ?
With respect to the hypothesis that MdDS is caused by reweighting of visual, vestibular or somatosensory input, the data so far is contradictory. Nachum and associates used posturography to study young males aged 18-22 with motion sickness and land-sickness (they considered land-sickness to be equivalent to mal de debarquement in their paper -- see table 2 above). They reported that these young men developed increased reliance on somatosensory input after motion exposure, and reduced weighting of vision and vestibular input (Nachum, Shupak et al. 2004). While the accuracy of visual input depends on whether one is inside the boat or on the deck, semicircular canal input is accurate on boats, and somatosensory input is intermittently accurate. Accordingly, it is difficult to understand a rationale for this adaptation. An intrinsic problem with this study is that the study group were young men with motion sickness and transient land-sickness, not middle aged women with the month-or-greater MdDS syndrome.
Stoffregen et al (2013) also studied a different group than the usual MdDS sufferers -- 40 students of average age 20.68 years, oddly enough, without reporting their gender. Like Naichum et al, they defined MdDS to be landsickness, and thus they were studying something other than MdDS, but calling it MdDS. They defined "Low-MD" as symptoms for 30 minutes or less, and "High-MD" as symptoms for 120 minutes or more. Because this paper's definition of MdDS and subject population is so different than the clinical population in which the medical community diagnoses MdDS, they were studying landsickness but they were calling it MdDS, and there is little to be gained in considering their work further. It is interesting to note that their paper was published in Plos, an open source journal. While the PLOS journals are very accessible, their review process is quite different than the traditional one that involves experts in the field. In other words, publications in PLOS carries less weight than publication in a standard journal.
Well, at any rate, rather than the somatosensory weighting process suggested by Naichum, a more reasonable possibility is that individuals with MdDS may develop an increased reliance on visual and vestibular information (and thus decreased somatosensory weighting). This occurs in normal subjects who are exposed to situations where somatosensory feedback is distorted (Peterka, 2002), and would also be a reasonable adaptation to boat pitch. Either adaptation might result in inaccurate land sensorimotor integration. Nevertheless, neither of these adaptations explain the rocking sensation of MdDS or the characteristic improvement on driving a car.
The most recent mechanistic proposition for MdDS is that of Dai and associates (2014). They proposed that MdDSs was caused by maladaptation of the vestibulo-ocular reflex (VOR) to roll of the head during rotation, and reported that a 5 day long protocol attempting to readapt the VOR resulted in “substantial recovery on average for approximately 1 year” of 17 of 24 subjects. While these results are encouraging, this theory does not explain why patients with MdDS are better while driving. Furthermore, it is difficult to see why ordinary movement through the environment should not recalibrate the VOR over a few days – the usual upper limit for the duration of land-sickness. At the time of this writing in 2015, the roll adaptation theory and treatment protocol needs more study.
In our opinion, the diagnosis of MdDS is made by a combination of the history (rocking after prolonged exposure to a boat or other source of prolonged motion), improvement with driving, and exclusion of reasonable alternatives. A motion exposure of 2 hours is a bare minimum. The typical duration of exposure is a week. Tests to exclude Menieres disease should be done (i.e. hearing tests) and vestibular neuritis (usually bedside testing is enough), and if there is a history of plane flight, perilymph fistula should also be considered.
Ombergen et al (2015) suggested similar diagnostic criteria:
Ombergen et al (2015) did not include improvement on driving in their criteria, but otherwise these seem quite reasonable.
A typical patient is a woman between 40-60 years of age, who has gone on a cruise, and who is now rocking. Recently, the criterion has been expanded to require getting better on driving. This feature is extremely common in MdDS, but rare (but not at all unheard of) in inner ear disorders or Migraine. (Sharon and Hullar, 2014)
Testing in Mal de debarquement:
Cohen et al (2015) state that "although vestibular testing can be of use, in general, MRIs, VEMPS, auditory evoked potentials and multiple blood tests really have nothing to offer diagnostically". That being said, MRI's are commonly done.
Gibbs et al (2010), determined that the Romberg test is not sensitive to "sea legs" (landsickness). This is very puzzling given that a prominent complaint is imbalance. It is also puzzling in that our treatment results which includes posturography suggests improvement in balance with reduction of rocking. Perhaps the Romberg test variant used by Gibbs et al (2010) was just too easy. Generally one can always find a Romberg variant that is difficult for someone.
In our practice, we get the following tests, in persons who are not "classic" (i.e. "rockers") -- i.e. not improved by driving and not on a cruise, see table 1:
We have not found that MdDS patients exhibit abnormally large vestibular gains or abnormally long time constants on rotatory chair tests. They generally test normally on the rotatory chair, unless they are taking benzodiazepines such as klonazepam or diazepam (which decrease VOR gain and increase VOR time constants).
- Audiogram and sweep OAE (expect normal, abnormal suggests other disorders involving injury to the ear)
- Rotatory chair test. This is usually shows normal vestibular responses. The VHIT test is sometimes used instead of the rotatory chair, but it usually provides less information. The advantage to the VHIT is that it is unlikely to be associated with motion sickness.
The usual treatment strategy for MdDS is to attempt to make the patient comfortable, while waiting for the MdDS to end by itself (typically within 6 months, see table 1). If "waiting it out" doesn't work, then a recent development is that some patients go for roll-adaptation (see below).
After MdDS has started, most medications that work for other forms of dizziness or motion sickness are ineffective. Specifically, antivert (bonine, meclizine), dramamine, and scopolamine seem to be of little use. The author has tried out many other medications, and has also not found response to more unusual agents for dizziness such as betahistine, baclofen, or verapamil.
Conventional vestibular suppressants that affect anticholinergic pathways such as meclizine and transdermal scopolamine are not helpful in MdDS. (Hain, Hanna et al. 1999) Benzodiazepines, such as clonazepam, are of the most benefit. (Hain, Hanna et al. 1999; Cha 2012), and SSRI type antidepressants are also suggested as being potentially helpful (Cha 2012). There are also anecdotal reports of good responses to gabapentin, amitriptyline, and venlafaxine. Others have reported that nortriptyline is helpful. All of these are medications that are also helpful in migraine.
We do not see that MdDS should generally be a reason to pull someone's drivers license, as generally MdDS symptoms remit entirely while driving.
- Low doses of clonazepam, a benzodiazepine medication related to Valium (diazepam), are helpful in most persons with MdDS. There is some worry that these medications may prolong the duration of symptoms (although this worry has not yet been tested by a research study). These medications increase GABA. These benzodiazepine medications are also addictive, which is worrisome. We do not favor constant use of klonopin for MdDSs. Rather, we usually suggest occasional "emergency" use.
- We have also had some recent success with treatment with venlafaxine - -this is an antidepressant that is very useful in migraine. We use the same protocol as for treatment of migraine (top dose typically only 37.5 XL). Others have reported (in 2016 at COSM meeting) that treatment with migraine medications (e.g. nortriptyline, verapamil) is successful in about 60% of the time. This needs more investigation.
- Occasional patients have reported improvement from treatment with Neurontin (gabapentin). This is generally in very large doses (e.g. 2400 mg, although one would think that 900 would be plenty). We don't prescribe this anymore for MdDSs because we think the side effects exceed the benefits.
- We have also had occasional patients respond to tiagabine (Gabatril) (another gaba medication - there is a theme here !)
- Occasionally persons with rocking due to other causes respond to one of the SSRI type antidepressants, and this may also be worth considering. Paroxetine is the most common SSRI used in persons with dizziness.
- Somewhat similarly to venlafaxine, as of 2014, there are a few reports of a good response to Sinemet, which the brand name of a medication (carbidopa-levodopa) that increases dopamine. As dopamine is a precursor to many neurotransmitters, including norepinephrine, increased dopamine may be working downstream to increase the levels of these neurotransmitters. It seems unlikely to us that dopamine deficiency is the cause of MdDS, as there is an immense population of people with dopamine deficiency (i.e. Parkinson's patients), that hugely exceeds the number of people with MdDS or rocking.
- "One-off" treatments -- we are not sure, would be interested if others have had a good or bad effect.
- We have been told that non-steroidal anti-inflammatory medications have helped MdDS, but this does not seem to be a general pattern. Perhaps the mechanism here is quieting down migraine.
- phenytoin and carbamazepine (or oxcarbazepine) may be useful in reducing symptoms. Phenytoin has been reported useful in motion-sickness. A controlled trial of these medications may be in order if more evidence accumulates.
- We have been told that the "non-THC" form of medical marijuana was helpful in one case. Again, more reports are needed.
Medications to stop and procedures to consider stopping.
|Figure 4 from Dai et al, 2017, showing percentage of patients with a reduction of 50% or more on symptom score, as a function of time after treatment.|
Dai et al (2014) reported successful treatment of MdDS in about 60% of cases using a procedure involving optokinetic visual stimulation and tilting of the head about the front-back axis (roll). The procedures involves multiple short sessions over a week. The study was uncontrolled. According to Cohen et al (2015), more than 100 patients have been treated wit this protocol, and the "cure rate" is similar to the original report (about 60%). A recent follow-up (Dai et al, 2017), reported outcomes in 141 patients (122 females, 19 males). Their criteria for "significant improvement" was a reduction in the score on a symptom questionnaire by 50% or more. Patients were categorized as "classic" or "spontaneous" MdDS. They reported "significant improvement" in 78% of "classic MdDS", and 48% of "spontaneous MdDS". At one year, "significant improvement was maintained in 52% of classic, and 48% of spontaneous patients". They found that success was "generally inversely correlated with the duration of the MdDS symptoms and with the patients' ages".
This protocol and result has been replicated in about 25 patients at Chicago Dizziness and Hearing. As noted above, we are dubious that roll adaptation explains MdDSs, and for this reason we are also dubious about the rationale for this treatment. Still, it seems harmless and given that it seems successful both in New York as well as in our clinic, we think it reasonable to try in MdDS patients that have not resolved with time. We are presently treating patients in our dizzy practice in Chicago.
Recent reports by Dai and colleagues (2017) suggest that the optokinetic treatment is more successful in the classic motion triggered "MdDS", than the group variously called "rockers" -- also known as "spontaneous" MdDS, or non-motion triggered MdDS (which is an odd construction -- lack of motion triggering for a syndrome named for "debarquement"). The initial rate of success is higher in persons who have had it for shorter times (e.g. 1 year as opposed to 3 years).
After treatment, Dai et al (2017) found that there was partial regression, particularly in the "spontaneous" group, over about a year (see above for results in the "classic" MdDS group, that did better than the spontaneous).
|Bertec VR device.||Gyrostim device.|
We are doubtful that there any "quick fixes" to MdDS, and we would expect any successful protocol would entail a lot of exposure to motion, and discomfort from motion sickness. With that idea in mind, lets consider some new gadgets out there.
Recently equipment companies have released devices with "MdDS" protocols. For example, Bertec has a MdDS protocol in their very cool looking balance device, dynamic CDP. This device appears to be basically a visual stimulator with a posture platform underneath it. It is probably better than the TV array (that we use in our clinic), or the OKN drum (used by Dr. Dai), as it is more "immersive" than our flat screen, and it does more axes (than the drum). We don't see why the posture platform is helpful. We were disturbed in interviewing an MdDS patient who told us that this device was being used for treatment (not very successful), using a 3 times/week 1 hour protocol. To us, this seems to be not enough. Our thought is that any "device" based treatment, that is successful, will take a lot of time (i.e. half of a week, full time), and because it "locks down" both the patient and the room and the device, be very costly. We don't think there will be any one hour treatments and cures, or for that matter, series of 1 hour treatments 3 times/week for 8 weeks with cures.
A very wild looking device is called "GyroStim", which appears to be something similar to a carnival ride. It resembles a ride we took once at Epcot. It seems to do both Yaw and pitch. In other words, it is a "pitch while rotating" device. It doesn't seem to have any optokinetic component. The old literature on these stimuli suggests that they are very nauseating (Raphan et al, 1983; Rapahn et al,1999) . Our take on these is that anything that provides multi-axis visual-vestibular stimulation will probably habituate the vestibular system, and has a reasonable chance of helping MdDS, although there is also a high likelihood of causing nausea and vomiting. So we would think the device might work, but the issue would be tolerability, and also because this device looks pretty fancy, high cost. We are a bit dubious that this device can be used to treat MdDS for patients requiring 4 hours of treatment/day for a week. But perhaps we are wrong. We also would be worried about vomiting. We are dubious that one could take meclizine and get any benefit out of this device.
We suspect that simpler approaches, such as the home MdDS treatments that we provide some software to help with, or the "PUMA" exercises, might be as effective, given that one is willing to put up with a lot of nausea. We also think that a VR type device (now they are down to about $200/oculus rift), combined with an active head movement protocol, might be fairly cost effective. We think that what matters is how much you can reasonably stimulate the vestibular system, without having the person "bail" due to nausea. Protocols that gradually "ramp up" exposure, would seem fairly logical.
Another issue is that, of course, unlike the Dai protocol that has 2 papers as well as our clinic's experience regarding success, these devices have no track record at all, they are expensive, using them locks them down for a long time, and somebody obviously has to pay for this. We would like to see the results of a series, especially on the Gyrostim devices including roughly 20 MdDS patients, preferably with a placebo control. Without significant funding, it seems a bit unlikely.
Neither of these devices combines multi-axis with visual stimulation. Combine Bertec with Gyrostim. So there is still room for more gadgets ! We would think that the military must have these things (they are called flight simulators).
Repetitive transcranial magnetic stimulation (TMS) over the dorsolateral prefrontal cortex was reported by Cha to be associated with “short-term symptom improvement”, in a pilot study of Cha in 2013 as well as helpful in 5 of 10 subjects in more recent studies of Guofa et al (2015) and Pearce (2015). More study is needed of this treatment modality for MdDS. In TMS, generally any changes are temporary. For example, although TMS can be used to treat depression, one needs to do it over and over again every week. A treatment protocol that accomplishes long term improvement in this disorder that lasts months to years is crucial. See our "exciting stuff" page concerning our attempt to find a provider for TMS for MdDSs patients in Chicago.
Dai et al (2017) commented that "Since the process producing the MdDS most likely originates in the velocity storage mechanism in the brainstem, magnetic cortical stimulation is likely to be ineffective in producing long-term relief." Our perspective on this comment is that in reality, we don't think the "process producing the MdDS" has been clearly identified, but given that in TMS changes are generally temporary, the timing comment is likely correct.
Medications taken prior and during boat travel might prevent development of MdDS.
Physical therapy: The evidence for a positive role for physical therapy in MdDS is somewhere between nonexistent and weak (Hain and Helminski, 2007). In our original study of MdDS (Hain et al), 10/15 persons who had vestibular rehabilitation reported improvement, but the natural history of MdDS is to improve, and one wonders what would have happened had they not undergone rehabilitation. In other words, this was an uncontrolled study, which sheds no light on whether PT is helpful. Cha commented in passing that "only rare patients seem to be cured by vestibular therapy" (Cha 2012). In fact, the only peer reviewed literature describing physical therapy treatment for MdDSs are two case reports (Zimbelman and Watson 1992; Liphart et al, 2014). Of course, it is not known how these cases would have done without PT. In other words, these were not controlled. In general, while many individuals with MdDS undergo vestibular rehabilitation, again because of a lack of controls, it is not possible to determine whether they did any better than persons who were not treated (Hain, Hanna et al. 1999). Thus the efficacy of vestibular rehabilitation for MdDSs is unknown.
Motion sickness has been treated successfully with habituation (Dai, Raphan et al. 2011), and one might reasonably argue that MdDS, being a motion sickness variant, might also respond to a similar approach. Habituation entails a down-weighting of motion input, and can reduce the long duration vestibular responses commonly associated with motion sickness susceptibility (Dai, Raphan et al. 2007). Although there are well developed self-directed motion habituation protocols such as the PUMA exercises (Puma 2010), there are presently no published reports of their efficacy in MdDSs (or motion sickness for that matter). Nevertheless, we are sympathetic to the general idea that things that make you feel worse (when you are dizzy) usually does result in some improvement (if you can stand it). The Puma protocol exercises are just so extremely stimulating that so far -- nobody has been able to tolerate them for more than a session or two. The Puma protocol exercises can be bought on the web in the form of a DVD from Dr. Puma's website.
The roll adaptation protocol of Dai et al (2014) could be reasonably viewed as a type of habituation. We offer this treatment in our practice in Chicago. Our view based on a substantial experience, is that it does help. Nevertheless, it is time intensive and we think only suitable for severe cases.
While we find this idea very doubtful, if MdDS is indeed due to inappropriately high weighting of somatosensory input, vestibular physical therapy protocols that teach down-regulation of somatosensory input seem worth trying. Liphart (2015) reported results of "sensory reweighting therapy in a single atypical case. The single subject "felt she had improved 50%". This is not too different from results of roll adaptation discussed above. A controlled trial of vestibular rehabilitation in a large number (i.e. 20) of MdDS subjects could be helpful in clearing up this question (hope someone funds this !). Our guess is that results of vestibular rehabilitation treatment would not be any different than no treatment.
If MdDS is instead caused by an internal oscillator developed to predict boat motion, one's treatment strategy should be aimed at manipulation of psychological variables rather than somatosensory integration. Patients need to ignore their aberrant internal signal, in the same way that most persons with tinnitus eventually develop an ability to ignore abnormal internally generated sounds. Treatments that decrease vigilance, obsessiveness, and anxiety as well as "tincture of time", would be the optimum strategy. CBT (a form of psychotherapy) is often successful in treating tinnitus. We are not aware of this approach being tried for MdDS. Against this general idea is that the roll adaptation treatment discussed above does seem to work.
Going on another boat and related activities:
MdDS is not very well studied. Considering that many other obscure conditions have 1000's of papers written about them, this means that MdDS has been generally ignored.
There are many open questions. Here are a few:
- Controlled trial of medication(s) for MdDS. Is clonazepam effective ? How about anticholinergics ? Antihistamines ? phenytoin ? oxcarbamazine ? gabapentin ? (our guess -- clonazepam is effective, none of the others are reliable or significant).
- Does regular use of benzodiazepines (such as clonapin) prolong the duration of MdDSs ? While a few animal studies suggest that these medications reduce adaptation, human studies so far don't. We just don't know. The evidence is not strong.
- How does MdDS and migraine interact ? Do medications for migraine reduce probability of MdDS ? (our guess - -certain ones -- venlafaxine - -might help)
- What factors affect duration of MdDS ? Does ongoing motion exposure that alleviates symptoms (i.e. driving) slow down recovery ? (our guess- - yes)
- Role of physical therapy (if any) in MdDS ? Compare vestibular physical therapy to strength training (for example). (our guess -- PT doesn't help)
- Role of psychotherapy (if any) in MdDS ? Cognitive behavioral therapy is often helpful for tinnitus -- perhaps MdDS is somewhat of a vestibular tinnitus (our guess - -probably helpful in some-- CPT is powerful).
We know of three ongoing research projects regarding MdDS, two treatment projects in Oklahoma (Dr. Cha), another in Ohio(Dr Clark).
We do not know of any treatment projects involving medication. The following are some recent links.
There is a MdDS foundation, which maintains it's own website and encompasses a quite active group of volunteers. The author of this page, Dr. Hain, is loosely associated -- I sometimes provide some advice to this group. There are also several other groups world-wide.
Note that many of the references regarding MdDS are from lesser sources -- "open access" journals, review articles, articles for the public. Not much data here.
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