Halasy, Michael P. MS, PA-C, DHSc; Thibault, Christopher R. DPT
A 40-year-old woman presents to the ED with the complaint of a 16-day history of worsening disequilibrium and dizziness. The patient states that she was vacationing in California and returned 9 days ago. She says that because of previous issues with motion sickness, she carries scopolamine patches and uses them as needed when traveling to prevent motion sickness. Before her plane's initial departure, she applied one to her right shoulder. Upon arriving at her destination in California, she began to experience feelings of motion sickness and dizziness that she attributed to driving on “curvy roads.” These feelings continued throughout her vacation. Before leaving for her return flight, she applied another scopolamine patch to her right shoulder, and noted that her symptoms improved during her flight home, but thought that this was likely secondary to the scopolamine. She has used scopolamine in the past and has had some residual fatigue and blurry vision, but had not experienced symptoms like this.
Upon ED presentation, she notes photophobia, phonophobia, black floaters, and a feeling of being “disconnected” from everything around her. She works at a desk, and notes that since her return, she has experienced waves of nausea and vertigo. When she attempts to work on her computer, she feels like she is in a fishbowl. She has a recent history of breast cancer and is in remission, but wonders if she should be concerned about an intracranial lesion based on her symptoms. She has never had symptoms like this and is concerned about the possibility of a neurologic disorder such as multiple sclerosis or a stroke.
Physical examination The patient appears in no acute distress. She is alert and oriented to person, place, and time. A mental status exam was completed and was noted to be normal. Her head is normocephalic and atraumatic. A neurologic examination finds cranial nerves II through XII grossly intact, upper extremity strength intact bilaterally, and normal coordination (including finger-nose-finger, rapid alternating movements, and heel to shin). Upper extremity reflexes are normal and symmetric. Hoffman sign is negative, a sensory examination is normal, and tandem gait and Romberg sign are normal.
The patient's pupils are equal, round, and reactive to light and accommodation, extraocular movements are intact, and a fundoscopic examination is unremarkable. She has no spontaneous nystagmus, ocular smooth pursuit is normal, and tests of gaze holding nystagmus, saccadic eye movements, head thrust, vergence, bilateral roll, coordination, and dysmetria are all negative. Dix-Hallpike test also is negative. Vestibuloocular reflex cancellation is normal. Changing position increases the patient's symptoms but is negative for nystagmus and vertigo. The patient's cervical range of motion is within normal limits.
Initial diagnostic studies Initial laboratory workup consisted of an electrolyte panel and a complete blood cell count with differential to exclude metabolic and infectious sources. Test results were within normal limits. Because of the patient's history of breast cancer and her atypical presentation, a head CT was obtained and ruled out intracranial lesions.
Treatment plan An atypical cause was suspected for the patient's vertigo. Her symptoms were not concerning for central vertigo but not readily explained by common causes of peripheral vertigo. Additionally, she was quite anxious because of her history of breast cancer. While the patient was awaiting results of her head CT, IV access was obtained and 1,000 mL of 0.9% sodium chloride solution was started. She also was given IV promethazine 25 mg, diazepam 5 mg, and ondansetron 4 mg. Her symptoms improved while she was in the ED to the point where she felt safe to return home. An outpatient appointment was arranged for follow-up in the vestibular laboratory for further workup and examination. The patient was subsequently seen in vestibular laboratory 5 days after her presentation in the ED, but she had marked improvement in her symptoms with nearly complete symptom resolution. So although no formal diagnosis could be made, mal de debarquement syndrome was considered probable.
Dizziness remains one of the more common complaints seen in the ED, with an estimated 7.5 million visits annually; 54% of these visits are secondary to benign or peripheral vertigo. This patient presented with an interesting clinical scenario. Our initial assessment was unremarkable for central vertigo causes, and her symptoms did not fit any known peripheral vertigo pattern. Although unconfirmed, the above case presentation is suggestive of mal de debarquement syndrome, also known as the “sickness of disembarkment,” which occurs when the body's vestibular system becomes habituated with the rocking rhythmic movement of travel.
Mal de debarquement syndrome was formally described and increased in recognition following the work of Brown and Baloh in 1987.1 This syndrome usually occurs during shipboard travel on cruise liners but has been reported in air travel as well.1 Although mal de debarquement syndrome has some similarity to “landsickness,” the two can often be distinguished by two features:2
* Landsickness, also known as postmotion vertigo, rarely lasts more than 48 hours.
* Landsickness often responds to typical vestibular therapy such as meclizine.2
Mal de debarquement syndrome is resistant to readaptation to stable conditions, and people will often feel as though the ground is moving, and have a self-perception of rocking, bobbing, or swaying. Unusually, symptoms often resolve when patients again experience passive motion (such as the motion that initially caused the symptoms).2
The exact incidence of mal de debarquement is unknown; researchers believe that most patients do not seek medical care.3 Mal de debarquement is still poorly understood, but is thought to be a disorder of neuroplasticity and sensory rearrangement that does not appear to involve the vestibular system (vestibular testing is unremarkable and normal treatment programs for vestibular therapy do not help the underlying symptoms).4
Mal de debarquement can be a persistent disorder, and although most patients have rapid symptom resolution, some continue to have symptoms for some time.5 A retrospective review done in 1999 identified 27 patients with mal de debarquement, with a mean duration of symptoms of 3.5 years.2 Another study, however, noted that 51% of episodes lasted longer than 1 month, but less than 1 year.6 Some experts disagree as to whether mal de debarquement can be diagnosed in a patient who has had symptoms for less than 1 month, or if symptoms need to be present for a minimum of 1 month.2,7
Most cases spontaneously resolve without any particular treatment. For patients with persistent symptoms, however, treatment options are limited. Benzodiazepines offer the best symptomatic relief, with clonazepam often used because of its long half-life. Amitriptyline has modest benefit, and meclizine and scopolamine were found to be of no benefit.2 Selective serotonin reuptake inhibitors have been found very useful in a limited number of patients, and may provide some additional value.5
This patient had a challenging presentation, as her symptoms could not be localized to any specific peripheral vestibular cause. Although her symptoms resolved within 21 days and before confirmatory diagnosis with our vestibular laboratory, several items in her history point to mal de debarquement as the cause. First, she noted the onset of her symptoms after her initial flight; the symptoms persisted despite the scopolamine, but improved on her return flight. Secondly, she had used scopolamine extensively in the past with none of the current symptoms. Although anticholinergics and, in particular, scopolamine can cause adverse reactions, this cause seemed unlikely given the patient's history with the medication. Also, scopolamine had none of the desired effects on the vestibular system, as it normally would in a patient with peripheral vertigo. The patient also continually mentioned feeling “disconnected,” consistent with a cognitive dysfunction often seen in mal de debarquement, and almost never seen in peripheral vertigo. Some patients develop new-onset headaches with mal de debarquement, but this patient did not have these symptoms.8 Her presentation and clinical characteristics are consistent with an acute presentation of mal de debarquement syndrome with resolution by 3 weeks postoccurrence.
1. DeFlorio PT, Silbergleit R. Mal de debarquement presenting in the emergency department. J Emerg Med
2. Hain TC, Hanna PA, Rheinberger MA. Mal de debarquement. Arch Otolaryngol Head Neck Surg
3. Gordon CR, Spitzer O, Doweck I, et al. Clinical features of mal de debarquement: adaptation and habituation to sea conditions. J Vestib Res
4. Clark BC, Quick A. Exploring the pathophysiology of mal de debarquement. J Neurol
5. Cha YH. Mal de debarquement. Semin Neurol
6. Cha YH, Brodsky J, Ishiyama G, et al. Clinical features and associated syndromes of mal de debarquement. J Neurol
7. Teitelbaum P. Mal de debarquement syndrome: a case report. J Travel Med
8. Cha YH, Cui Y. Rocking dizziness and headache: a two-way street. Cephalalgia
© 2014 American Academy of Physician Assistants.