Timothy C. Hain, MD Page last modified: June 24, 2019
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 as it has been pointed out that "MDD" can be confused with other disorders.
Note that the MdDS of "Mal de Debarquement" has no connection to the MDD of "Major Depressive Disorder". One 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.
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. Van 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. In our practice's clinic database, we have more than 250 patients ourselves.
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 first 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 Van 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. As of 2019, we have accumulated a few more than 250 patients with MdDS in our files.
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 pulling", and "trampoline walking". They had a sway frequency that was predominantly 0.2 Hz. This is very slow -- with a full cycle occurring 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 2019, we had encountered 258 MdDS patients in our dizzy clinic database out of an "n" of about 25,000 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), MdDS 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. This is very relevant because papers in the field that have "Mal de debarquement" in their title, are often studies of land-sickness. Sort of a bait/switch technique, probably because land-sickness is much easier to study, but using the name of MdDS is more novel as the aerospace literature has plenty of land sickness articles.
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 (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). As mentioned above, LDS, is also termed "mal de debarquement" by many (e.g. Schepermann et al, 2019), presumably for convenience as LDS is much easier to study. 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", but some related publications from the same group mix them together.
Van 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 Van Ombergen et al (between 2-3 days). From 3 days to several years would overlap to some extent with the 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 et al. 1999; Cha 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. Another name for the same group is "non motion triggered MdDS"(Cha 2012) -- 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". The attitude in the literature seems to be that it is best just to tolerate these irrational nomenclatures.
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) also 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.
To start with, there are many unproven conjectures about the cause of MdDS. There is no "dominant" theory. If somebody tells you that MdDS is due to this or that, you should expect them to also say that this is just a theory, and that there are many other theories that could be true as well.
It is the general opinion that MdDS is generally not caused by an injury to the ear or brain. At this writing (2019), 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.
We will start with the more reasonable theories. Of course, more than one could be true at the same time.
Migraine: Many 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. Although it doesn't explain much, this is the best established theory.
Adaptation by down weighting vestibular: Another theory about the cause of MdDS it that is caused by inappropriately high weighting of somatosensory input for balance (Naichem et al, 2004). Your inner ear is giving you lots of information, so you increase your reliance on your feet. Still, as somatosensory information and vestibular information are both unreliable on a boat, this is a difficult explanation to follow.
Adaptation to roll while rotating (cross-coupling):
Another 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. A similar hypothesis was developed by Cohen et al (2018) -- from the same lab -- see next section.
Vestibular and cerebellar basis ?
Cohen, Yakushin and Cho (2018) published a hypothesis article in an open access journal (Frontiers), entitled "The vestibular and cerebellar basis of the mal de debarquement syndrome". They discuss animal research done in their lab -- of course animals don't get MdDS. Monkeys exposed to "roll while rotating", but not pitch while rotating, developed inappropriate nystagmus when rolled, for 18 hours. Roughly the same amount of time as land-sickness in humans. They call 18 hours "long lasting". One persons long-lasting might be another's short lasting. They are jumping here from 18 hours to 1 month -- not our idea of long lasting and certainly not in the same territory as MdDS (30 days to forever). So these authors propose a model of land-sickness. One would expect that any adaptation phenomenon would not persist forever, as if you can adapt one way, you can also reverse the process, usually much quicker than you acquired it.
This article goes on to discuss PAN, or periodic alternating nystagmus, which is a very slowly oscillating in appropriate eye movement that appears after brain damage (generally to the cerebellar nodulus). The author of this page has previously been a coauthor of several papers on PAN. (Chiu et al, 2002; Furman et al, 1989) They suggest that the timing of the oscillation of PAN is similar to the timing of MdDS. We agree -- it is even slower. Of course, the color of cheddar cheese is similar to the color of 24-caret gold, but one would not say that the two are otherwise similar. So the logical impact of this observation is limited. Of course, PAN is caused by a permanent process (damage to the cerebellar nodulus, often a tumor or stroke). It lasts forever, because the damage is there forever.
Overall, this article is relevant to land-sickness. It contains a large number of questionable assertions about MdDS and very wide-ranging conjectures. The core assumptions of this article are, as they say in the legal field, "hearsay" (unverified information). We are not at all against making hypotheses, but it is best to keep clear about what is established by verifiable evidence and what is not.
Internal model theory and MdDS
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 "down weighting" 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. In our view, this has to be an internal model problem.
The internal model theory explains most of the features of MdDS.
Hormones and MdDS:
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 menstrual period while on the boat. Mucci et al (2018) reported that "From the data collected, it was evident that naturally cycling female respondents from the MT group were significantly more likely to report an aggravation of MdDS symptoms during menses and mid-cycle (p < 0.001). " This would suggest that MdDS is triggered by estrogen fluctuations, similarly to Migraine and motion sickness.
As MdDS is rare in men, perhaps testosterone is protective. This idea is unproven and there are anecdotes on both sides of the issue.
At this writing (2019), there is quite a bit to be investigated about hormonal impact on MdDS.
Genetics: MdDS could also be genetic, related to two copies of the 'X' chromosome perhaps combined with other susceptibility factors. It is well known that there are motion sickness related genes. Out of more than 250 patients with MDDS, we have encountered only a single pair of identical twins who both developed MdDS (on different occasions).
Unlikely conjectures about MdDS:
Anxiety: MdDS 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) suggested that MdDS is due to "deafferentation" or panic. We disagree with both of these ideas. Certainly though anxiety could make MdDS worse (as it makes most illnesses worse).
Changes in the brain... 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".
Mucci, Cha and others al (2018) reviewed the neuroimaging studies (almost all due to Cha's work) in a "perspective" article in an "open access" journal, and suggested that the the change in brain connectivity was one of the "main theories". In this article, it is stated that the hypothesis involves "a disorder of abnormal functional connectivity driven by a central neural oscillator that becomes entrained during periodic motion exposure". The "central oscillator ... can toggle between high and low states", and "MdDS may be a disorder of over-synchronization of brain networks". We find these ideas interesting but vague. The separation between cause and effect -- i.e. is the change in brain function the cause of MdDS or a consequence, still seems to be missing. There is also the difficulty that high field MRI's induce dizziness themselves. We are not convinced by the observation in this article that nystagmus (eye movement) was not observed in their own subjects, as we think the physics involved in MRI are pretty straightforward.
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). Nonetheless, most MdDS patients did not withdraw from SSRIs.
The "Norwalk" virus is common on cruise ships, and perhaps this syndrome is somehow related to this virus. This seems a bit unlikely in that MdDS can follow motion exposure on a variety of vehicles other than boats, as well as the observation that Norwalk virus outbreaks such as in food borne epidemics on land, does not appear to be associated with MdDS symptomatology.
A recent hypothesis was offered that MdDS is related to an imbalance of CGRP. (Mucci et al, 2018). This is a bit hard to follow in as much as CGRP modulates vascular tone. Although there are now new drugs that inhibit CGRP for migraine headache., these monoclonal antibody based drugs do not generally get into the brain. Our expectation (as of 2019) is that these will not help MdDS, and at this writing, we don't think they are worth pursuing.
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 land sickness, 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 land sickness but they were calling it MdDS, and there is little to be gained in considering their work further. It is interesting to note that Stoffregen's 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 carry less weight than publication in a standard journal where the material is reviewed by experts chosen by their knowledge of the topic.
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; Cohen et al, 2018). They proposed that MdDS 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 2019, the roll adaptation theory remains unproven, and the reason why the treatment is partially successful remains uncertain. Habituation is the obvious alternative theory to readaptation. A recent report suggests that this procedure is better than placebo, but the direction of the optokinetic stimulation does not matter (Mucci et al, 2018). This would be in favor of habituation over readaptation.
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, a duration of at least 1 month, 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 BPPV, Meniere's disease (i.e. hearing tests) and vestibular neuritis (ideally VHIT testing), should be done and if there is a history of plane flight, perilymph fistula should also be considered.
Ombergen et al (2015) suggested similar diagnostic criteria:
- Chronic rocking dizziness that started after either passive motion or exposure to virtual reality (the virtual reality history is not supported in previous literature)
- Symptoms lasting for at least 1 month
- Normal inner ear function or unrelated abnormalities on ENG/VNG or audiological testing
- Normal structural brain imaging
- Symptoms not better accounted for by another diagnosis (this makes it a "wastebasket" syndrome, similar to vestibular migraine or PPPD).
Ombergen et al (2015) did not include improvement on driving in their criteria, but otherwise these seem quite reasonable. We think the improvement on driving should be included.
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. Note that the Ombergen criteria requires "structural imaging".
Gibbs et al (2010), determined that the Romberg test is not sensitive to "sea legs" (land sickness). 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 big advantage to the VHIT is that it is unlikely to be associated with motion sickness and also that it is a very good test for vestibular neuritis. .
We have moved this page elsewhere, as this page was getting too big. See the MdDS page in the treatment section of this site.
Medications taken prior and during boat travel might prevent development of MdDS.
Going on another boat and related activities:
MdDS is not very well studied. As of 2019, a search of Pubmed for titles including "mal de debarquement" in the title turned up only about 56 papers. Considering that many other obscure conditions have 1000's of papers written about them, this means that MdDS has been generally ignored.
Ongoing research projects regarding MdDS include several in Oklahoma (Dr. Cha), several by Dr. Mucci, some in Belgium (Van Ombergen), and in Ohio (Dr Clark).
Dr. Brian Clark, from Ohio University, is the lead investigator in a pilot study, Development of a Tele-medicine Approach for the Treatment of MdDS. This effort includes investigators from Ohio University, Ohio State University, and the Icahn School of Medicine at Mount Sinai in NYC.
We do not know of any treatment projects involving medication. The following are some recent links.
- An abstract concerning the research project in Ohio is here.
- A new survey of patients with MdDS has been offered by an Australian group. https://www.surveymonkey.com/r/MdDS_Survey_Browne
- Dr. Cha's email link is: MdDSResearch@laureateinstitute.org
- A study regarding pregnancy and MdDS from Western Sydney
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, and articles for the public. Not much data here. Note also that there is not much publication about MdDS.
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