Mal de Debarquement Syndrome

Mal de debarquement syndrome (MdDS) is a neurological disorder characterised by a persistent sensation of rocking, swaying or bobbing (non-spinning dizziness). It follows exposure to passive motion, or occurs spontaneously (without a motion trigger) in about 25 to 40 percent. It predominantly affects middle aged women.

Sea travel is the commonest trigger (80 percent). Other triggers are air travel, car and train travel, and prolonged flights.

A transient "land sickness" after travel is normal, lasting hours to days. MdDS is diagnosed when symptoms persist for more than 48 hours, and often for months to years (more than 1 month, up to decades).

About 80 to 90 percent of patients are women (mean age 40 to 50 years, with a link to menstrual cycle hormones and menopause). There is a strong link with migraine (about 50 to 60 percent have migraine, and migraine is a risk factor).

The pathophysiology is not fully known. It is thought to be a maladaptation of the vestibulo ocular reflex velocity storage and of central motion processing, with an entrainment of the motion perception system. Functional connectivity is abnormal in the entorhinal cortex, amygdala and cerebellum, along with increased metabolic activity in default mode networks. Positron emission tomography shows hypermetabolism in the entorhinal cortex and amygdala, with hypometabolism in the superior parietal region.

Typical features: the symptoms ease in motion (driving or passive travel in a car, boat or plane) and worsen when stationary. They can be associated with fatigue, brain fog, anxiety and depression.

• Constant sensation of rocking, swaying, bobbing, or being on a boat, lasting at least 48 hours, with a frequency of about 0.2 Hz; in up to 80 percent a feeling of "walking on a mattress".
• Symptoms are worse when quiet, standing still, lying, in enclosed spaces, and in visually busy environments (supermarkets, open spaces), and temporarily improve with passive motion (driving or riding in a car), with exercise in some.
• Associated: fatigue, headaches, difficulty concentrating ("brain fog"), anxiety, depression, hypersensitivity to light and sound, ear fullness, tinnitus, and sleep disruption.
• Symptoms may fluctuate with menstrual cycle, stress, and travel.
• Neurological and vestibular examinations are normal; no nystagmus; normal gait, Romberg may be abnormal in persistent cases.
• Substantial impairment of quality of life, work and social activity.

• Clinical diagnosis (consensus criteria): chronic non-spinning vertigo characterised by a subjective sensation of self-motion (rocking, swaying, bobbing) that began within 48 hours after the cessation of passive motion exposure and lasts longer than 48 hours.
• Symptoms are temporarily suppressed during passive motion. There is no other cause, with normal neurological examination.
• Exclude other conditions by history and testing: vestibular migraine, benign paroxysmal positional vertigo, vestibular neuritis, Ménière disease, perilymph fistula, cerebellar disease, anxiety disorders, medication effects, and cardiovascular and neurological causes.
• Also exclude persistent postural perceptual dizziness, which is typically induced by upright posture and visual stimulation, and not suppressed by passive motion.
• Investigations are normal and used to exclude other disorders: audiometry, vestibular tests (video head impulse test, caloric testing, rotary chair, vestibular evoked myogenic potentials), posturography, and MRI brain (normal); blood tests for anaemia, thyroid and glucose when appropriate.
• Symptom scores, such as the Dizziness Handicap Inventory, Hospital Anxiety and Depression Scale and migraine screening, are useful.

Treatment is largely empirical, with several options of varying efficacy; a multimodal approach is common.

• Education and reassurance that the condition is benign, with a good prognosis for those whose symptoms started recently (the first 6 months), and information about the poor response to usual vestibular medications.
• Medications (no approved drugs; evidence is limited):
  • Benzodiazepines are the most effective drug class for symptom suppression: clonazepam 0.25 to 0.5 mg at night, titrated to 0.5 to 1.5 mg daily in divided doses, or diazepam 2 to 5 mg two to three times daily (short term or intermittent use because of dependence, tolerance and sedation).
  • Selective serotonin reuptake inhibitors and serotonin noradrenaline reuptake inhibitors: venlafaxine 37.5 mg increasing to 75 to 150 mg daily, sertraline 25 to 100 mg daily, or paroxetine 10 to 40 mg daily, with benefit in about 50 percent, especially if anxiety, depression or migraine are present.
  • Migraine preventive therapy for patients with a migraine history: topiramate 25 to 100 mg daily, nortriptyline 10 to 50 mg at night, propranolol 40 to 160 mg daily, or verapamil 120 to 360 mg daily, flunarizine 5 to 10 mg at night, with reduction in symptoms in many.
  • Gabapentin 300 to 1,800 mg daily, and lamotrigine 25 to 200 mg daily, have been used.
  • Vestibular suppressants such as meclizine and antihistamines are generally ineffective for chronic use, and may delay compensation.
  • Hormonal therapy (oestrogen replacement in perimenopause) may help in cycle related patterns.
• Optokinetic stimulation therapy (the Dai protocol): a customised visual vestibular paradigm of a full field optokinetic stimulus (rotating dot field) with simultaneous head roll oscillations at 0.167 Hz (patients' head tilt in a roll with the optokinetic stimulus). It is performed over 4 to 5 consecutive daily sessions of 20 to 40 minutes.
• More than 70 percent of patients report benefit, especially when the onset was motion triggered and short duration. Symptom severity improves by 50 to 70 percent at 3 to 6 months, though some relapse and need re-treatment. It is available in specialised centres.
• Neuromodulation: repetitive transcranial magnetic stimulation and transcranial direct current stimulation over the dorsolateral prefrontal cortex or the occipital area have shown benefit in some trials.
• Vestibular rehabilitation therapy: customised, with graded exposure to motion, balance and gaze stabilisation exercises, and habituation; individualised with caution as some patients worsen with some exercises; cognitive behavioural therapy for anxiety and stress.
• Lifestyle: regular exercise, adequate sleep, stress management, avoid migraine triggers, and avoid excessive visual stimulation and passive motion triggers if unsettled.
• Prognosis: variable; many patients improve slowly over months to years, some are persistent for years; early treatment may improve outcome; support groups are helpful.