Mal de mer | definition of mal de mer by Medical dictionary Mal de mer | definition of mal de mer by Medical dictionary Related to mal de mer: mal de mar mal mal de Meleda symmetrical keratosis of the palms and soles associated with a dry, scaly thickening of the wrists and ankles. mal de mer seasickness . sea·sick·ness (sē'sik-nĕs), A form of motion sickness caused by the motion of a floating platform, such as a ship, boat, or raft. See kinesia . seasickness A permutation of motion sickness, which occurs when a susceptible individual is subjected to the pitching and rolling of a ship, especially at the extreme fore or aft of the vessel. sea·sick·ness (sē'sik-nĕs) A form of motion sickness caused by the movement of a floating platform, such as a ship, boat, or raft. Mal de mer | Article about mal de mer by The Free Dictionary Mal de mer | Article about mal de mer by The Free Dictionary Related to mal de mer: mal de mar motion sickness, waves of nausea and vomiting experienced by some people, resulting from the sudden changes in movement of a vehicle.

The ailment is also known as seasickness, car sickness, train sickness, airsickness, and swing sickness. The principal cause of the disturbance is the effect of motion on the semicircular canals of the inner ear, although other factors such as inadequate ventilation and fumes or noxious odors may contribute. Drugs are available that, when taken beforehand, prevent the occurrence of motion sickness. Motion Sickness a syndrome occurring in man and some animals as a result of rocking on the sea (seasickness), air turbulence and aerobatics (airsickness), or rapid driving over a winding, bumpy road. It is caused by prolonged stimulation of the vestibular apparatus of the inner ear and by the action of impulses that originate in the internal organs on the autonomic nervous system. The symptoms of motion sickness include fatigue, dizziness, headache, copious salivation, nausea, vomiting (which causes temporary relief), and the appearance of cold perspiration. Prolonged motion may cause loss of consciousness. Aeron and diphenhydramine are used to prevent and treat motion sickness; persons with a highly sensitive vestibular apparatus may take the drugs before embarking on an airplane or ship.

Vestibular training (special exercises that increase the stability of the vestibular apparatus) is also helpful in preventing the syndrome. REFERENCE Mal de Debarquement syndrome Timothy C. Hain, MD Page last modified: October 18, 2016 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). Some Cases: 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. General characteristics of MdDS 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. 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. 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. How common is Mal de Debarquement ?

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. What is and isn't MdDS ? Motion sickness and Land-sickness is not MdDS. Table 2: Features Distinguishing MdDS from Land-sickness (LDS) Yes No 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).

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". 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. What causes Mal de Debarquement ?

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 ? Because the condition 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). MdDS and MdDS 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 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 reacting to 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 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). 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. Diagnosis of Mal de Debarquement 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: Chronic rocking dizziness that started after either passive motion or exposure to virtual reality 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 Ombergen et al 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 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. In o ur 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: 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. 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 (which decrease VOR gain and increase VOR time constants). Treatment for Mal de Debarquement 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 . 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. 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.

Also anecdotally, 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 do not see that MdDS should generally be a reason to pull someone's drivers license, as generally MdDS symptoms remit entirely while driving. Medications to stop and procedures to consider stopping. Hormonal medications such as estrogen or progesterone might be problematic -- it might be worth a trial of stopping them if this is practical. We are uncertain whether physical therapy is helpful in MdDS. Our opinion is that it is not. In our opinion, none of the following has any reasonable role in treating MdDS Dangerous medications of any type Herbal medications Ear drops, magnets, sea-bands, rose-colored or prism glasses. New treatment reported using optokinetic stimulation. 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%). This protocol and result has been replicated in 17 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 MdDSs that has not resolved with time. We are presently treating patients in our dizzy practice in Chicago . Recent reports by Dai and colleagues suggest that the optokinetic treatment is far more successful in the classic motion triggered "MdDS", than the group variously called "rockers", or non-motion triggered MdDS (which is an odd construction). This suggests that they are different conditions, that have been wrongly lumped together. New treatment reported using TMS.

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. Prevention of MdDS Medications taken prior and during boat travel might prevent development of MdDS. According to Cha and others (2009), having migraine increases the probability of recurrent MdDS. It would seem logical that medications that prevent migraine might also modulate MdDS. We are presently looking at this situation in patients taking venlafaxine.

See comments above regarding mechanism and serotonin. Anecdotal evidence suggests that while antivert and scopolamine are ineffective, people can prevent MdDS by taking very small amounts of Valium, klonopin, or Ativan (lorazepam) prior to getting on the boat or airplane. The author has used this strategy in his patients many times with excellent results. The usual dose is 0.5 mg, at start of trip and every 8 hours. For cruises, once every 12 hours is sufficient. Again, this strategy has not been tested by a research study and a trial, perhaps controlled with one of the medications known not to prevent MdDS might be helpful. Nevertheless, medications which suppress the inner ear or block adaptation to inner ear signals might be useful. Some have suggested to us that exercises done prior to getting back on the boat might prevent MdDS. Given our present theory of mechanism, we would find this idea very implausible. We do not know of any examples of this working or not working. Physical Therapy for 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, 10/15 persons who had vestibular rehabilitation reported improvement, but the natural history of MdDSs 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. Against this general idea is that the roll adaptation treatment discussed above does seem to work. Our suggestions for physical activity: Avoidance of periodic motion is probably helpful (Teitelbaum, 2002). If you get dizzy from riding on boats, don't do it ! We also tentatively think that large amounts of driving would be a bad idea. Internal model theory would suggest that it would be better to be a passenger than a driver (to prevent MdDS), but again, this is not established. Going on another boat and related activities: Well -- if you must go on another cruise for some reason, we advise taking small amounts of klonopin during the cruise (see "prevention" above). Situations where there is a direct confrontation between the rocking sensation of MdDS and a very clear and normal sensorium seem reasonable. In other words, walking outside (on a calm day), on a firm surface, where you can see the horizon, might be helpful.

Doing things that makes the symptoms better (such as driving a car for long periods), might (in theory anyway) prolong the duration of MdDS. Research is needed ! MdDS is not very well studied. As of 2015, only 52 papers came up on a "Pubmed" search for "mal de debarquement". 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 animal studies suggest that these medications reduce adaptation, human studies so far don't. We just don't know. 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) We know of three ongoing research projects regarding MdDS, two treatment projects in Oklahoma (Dr. Cha), another in Ohio(Clark). We do not know of any treatment projects involving medication. An abstract concerning the research project in Ohio is here . Related 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. Vestibular Disorders association (VEDA) References on Mal de Debarquement Syndrome 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. anonymous.

Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Headache Classification Committee of the International Headache Society. Cephalalgia. 1988;8 Suppl 7:1-96. Barmack, N.H. and H. Shojaku, Vestibularly induced slow oscillations in climbing fiber responses of Purkinje cells in the cerebellar nodulus of the rabbit. Neuroscience, 1992. 50(1): p. 1-5. Blakemore, S. J., et al. (1998). "Predicting the consequences of our own actions: the role of sensorimotor context estimation." J Neurosci 18(18): 7511-7518. Brown JJ, Baloh RW. Persistent mal de debarquement syndrome: a motion-induced subjective disorder of balance. American Journal of Otolaryngology. 1987;8:219-22. Cha, Y. H., J. Brodsky, et al. (2008).

"Clinical features and associated syndromes of mal de debarquement." J Neurol 255(7): 1038-44. Cha, Y. H. (2009). "Mal de debarquement." Semin Neurol 29(5): 520-527. (This is a collection of review articles). Cha, Y.H., Less common neuro-otologic disorders. Continuum (Minneap Minn), 2012. 18(5 Neuro-otology): p. 1142-57. (Continuum is a collection of review articles, and is not original research). Cha YH, Cui Y, Baloh RW. [ABSTRACT] Repetitive Transcranial Magnetic Stimulation for Mal de Debarquement Syndrome., Neurotology. 2012 Nov 29. Cha, Y.H., Y. Cui, and R.W. Baloh, Repetitive transcranial magnetic stimulation for mal de debarquement syndrome. Otol Neurotol, 2013. 34(1): p. 175-9. 25.

Cha Y, Chakrapani S, Craig A, Baloh RW. Metabolic and Functional Connectivity Changes in Mal de Debarquement Syndrome PLOS, 2012 (This is an open access journal) Cha, Y. H. and S. Chakrapani (2015). "Voxel Based Morphometry Alterations in Mal de Debarquement Syndrome." PLoS One 10(8): e0135021. (This is an open access journal) Cohen H. Vertigo after sailing a nineteenth century ship. Journal of Vestibular Research. 1996;6:31-5. Cohen, B., Dai, M., Smouha, E., & Cho, C. (2015). Mal de debarquement syndrome. Neurology: Clinical practice, 369-370. Dai, M., T. Raphan, and B. Cohen, Labyrinthine lesions and motion sickness susceptibility. Exp Brain Res, 2007. 178(4): p. 477-87. Dai M, Rapan T, Cohen B.

Adaptation of the angular vestibulo-ocular reflex to head movements in rotating frames of reference. Exp Br. res (2009) Dai, M., T. Raphan, and B. Cohen, Prolonged reduction of motion sickness sensitivity by visual-vestibular interaction. Exp Brain Res, 2011. 210(3-4): p. 503-13. Mal de Mer Mal de Mer Advice Sheet from the UK Sport Diving Medical Committee Scopolamine The most effective preventative for motion sickness, transdermal scopolamine, is now back on the market. Here are some products listed: Allscrips Transderm-Scop 1.5mg/72hr Ciba Pharm. Co. Transderm-Scop 1.5mg/72hr Novartis Consum Transderm-Scop 1.5mg/72hr Pharmedix Transderm-Scop 1.5mg/72hr . Side effects of scopolamine Scopolamine must be used with caution in people with glaucoma and benign prostatic hypertrophy and can cause hallucinations, confusion, disorientation and memory disturbance.

Other drugs Other less effective drugs include combinations of antihistamines and dextroamphetamine, Dilantin, nifedipine and ginger root. Use of dextroamphetamine is to counter the sedative effect of phenergan with which it is used in combination. Some believe this the BEST "mal de mer" medication. Single component drugs Scopolamine Hydrobromide (Transdermal ) The use of the wrist band has been found to be useless in at least one good study, but many swear by it and the "placebo" effect of a doctors recommendation sometimes works wonders. The FDA has approved it's use for motion sickness - but it is not water proof and this would appear to make it relatively useless to divers. Or, buy or make seasickness bands. They are merely elastic straps you wear around the wrists which press an acupressure point that is supposedly marvelously effective in preventing motion sickness. Other Remedies Try to sit amidships on the water, view the horizon, lean back against a firm surface and avoid neck movement. Try to suit up as quickly as possible and be the first in the water. The effects of motion gradually tend to wear off as time passes on the boat.

Former 'TravelWell' Audio Tapes now in CD format as 'Nevasic'. The product is now in the more favoured format of a CD and it's popularity has sharply risen due to that. As the product does not only deal with seasickness - we have disposed of the "purely a seasickness remedy" image and upgraded to a more appropriate name that deals with the symptoms of nausea and vomiting - nevasic. nevasic is also the core programme that the National Health Service in the UK researched with pregnant women (under the branded name MorningWell) - the results proving an over 90% success rate in reducing or alleviating the symptoms of nausea and vomiting in pregnancy or "morning sickness". Ginger About 1 gram of powdered ginger has been shown effective against motion sickness in double-blind studies. In Germany, up to 4 grams per day is recommended. Start dosing the night before a dive; the beauty of the ginger is it's easy to obtain and had no side effects. You might try gingersnap cookies instead. Ginger root works just as well as the tablets or powder. Ginger ale can also be used. Japanese food marts sell pickled ginger slices that can be used for the same purpose.

Ginger: Non-toxic Anti-Emetic Botanical Name: Zingiber officinale Plant Part Used: The rhizome Active Constituents: The dried rhizome contains approximately 1 to 4% volatile oils. The aromatic principles include the sesquiterpene hydrocarbons zingiberene and bisabolene. The pungent principles include the gingerols and shogaols. Actions on the Digestive System: Classified as an aromatic bitter, ginger stimulates digestion. It is also noted for improving gastrointestinal motility. 1. Ginger also improves the production and secretion of bile from the liver and gallbladder. 2. Ginger also qualifies as a carminative herb. Animal studies in Saudi Arabia show that ginger protects the stomach from the damaging effect of nonsteroidal anti-inflammatory drugs (ibuprofen is an example) and alcohol. 3. Ginger is a noted anti-emetic. While most research has suggested that this action is centered in the GI tract in humans, recent animal studies suggest that there may be some action on the central nervous system also. 4. Health Care Applications Motion Sickness: Ginger has been widely studied as a treatment for motion sickness.

A 1982 study found that ginger was superior to dimenhydrinate for reducing motion sickness (caused by rotating a chair). The dose of ginger was 940 mg and it was consumed 20 to 25 minutes before the test 5. A handful of studies since have both agreed and disagreed with these results. One study tested ginger against seasickness in eighty Danish naval cadets unaccustomed to sailing in heavy seas. One gram of ginger reduced vomiting and cold sweating. Fewer symptoms of nausea and vertigo were also reported. 6. A study completed at Louisiana State University with a grant from NASA is more skeptical. Because motion sickness is common in astronauts, the researchers compared the anti-motion sickness activity of ginger and scopolamine (commonly used as a topical patch to treat motion sickness). Using the rotating chair test, they found that scopolamine was effective in reducing motion sickness while one gram of either fresh or dried ginger was not. 7. However, during their discussion of the study, the authors note that the ginger group did have a noticeable reduction in the incidence of vomiting and sweating but not nausea and vertigo. Medline References for ginger.

Honey You might also like to try a spoonful or two of honey (take creamed honey when traveling, as the runny stuff gets everywhere). Phenytoin (Dilantin) Several divers have written about the effectiveness of Epanutin (TM), a brand of phenytoin, (Dilantin in the US). This drug is used and approved for the control of seizure activity. Dosage has not been developed for the medication to be used for seasickness - although reports from divers indicate that it be taken the night before the dive. (South Africa). There have been several studies where a single dose of phenytoin [200 mg] was given to volunteers who where then spun around. It seems there was a significant decrease in incidents of nausea in those subjects that were given the phenytoin. It seems that it acts on the nervous system of the digestive tract to decrease nervous activity associated with nausea. That was the good news, here the is bad news: 1. Phenytoin is a prescription drug here in the United States, you can't just drop by the local pharmacy and pick some up. 2.

It has some side effects that would be adverse to scuba diving should they occur at depth. These include ataxia, slurred speech, blurred vision, nystagmus, mental confusion, hallucination, headache and dizziness. Thus, it would be advisable for the diver to have 'tested' his/her reaction to the medication before the dive. These side effects may not show with just a single dose, but the actions of this drug combined with the effects of nitrogen narcosis need to be considered. 3. There are many drug interactions with phenytoin. Taking this drug while using other medications may produce the side effects that I mentioned above. In the U.S. its trade name is Dilantin. However, this drug is approved for epilepsy and not for sea sickness. References: Medline References about dimenhydrinate. Disclaimer Diving Medicine Online' does not endorse any of the medications, products or treatments described, mentioned or discussed in any of the services, databases or pages accessible within or from 'Diving Medicine Online', and makes no representations concerning the efficacy, appropriateness or suitability of any such products or treatments.

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Question: Mal de mer is the French term for which ailment in humans?
Answer: Seasickness