bims-madeba Biomed news
on Mal de débarquement syndrome
Issue of 2018‒11‒11
four papers selected by
Jun Maruta
Mount Sinai Health System

  1. Front Neurol. 2018 ;9 887
    Mucci V, Perkisas T, Jillings SD, Van Rompaey V, Van Ombergen A, Fransen E, Vereeck L, Wuyts FL, Van de Heyning PH, Browne CJ.
      Introduction: Mal de Debarquement Syndrome (MdDS) is a condition characterized by a perception of self-motion in the absence of a stimulus, with two onset types: Motion-Triggered and Spontaneous. Currently, the pathophysiology is unknown and consequently, the therapeutic options are limited. One proposed treatment protocol, developed by Dai and colleagues is based on optokinetic stimulation, which aims to re-adapt the vestibular ocular reflex. This study aimed to reproduce the treatment protocol developed by Dai and colleagues and to assess if a placebo effect is present in the treatment protocol and lastly, aimed to further investigate the treatment on MdDS patient outcomes. Method: Twenty-five MdDS patients (13 Motion-Triggered and 12 Spontaneous) were exposed to 5 consecutive days of optokinetic treatment (consisting of exposure to optokinetic stimuli with head movements). Eleven of these 25 patients were also exposed to 2 days of a sham treatment prior to the OKN treatment. Posturography measurements and reported symptoms [e.g., using the visual analog scale (VAS)] of patients were assessed throughout the treatment. Posturography data of the patients was compared with the data of 20 healthy controls. Results: No placebo effect was recorded with any changes in postural data and VAS scale. After the optokinetic treatment, a significant improvement in postural control was observed in 48% of patients, of whom 70% were of the Motion-Triggered subtype (p-values: Area under the Curve-Anterior Posterior < 0.001; Area under the Curve-Medio Lateral p < 0.001, Confidence Ellipse Area (CEA) < 0.001, Velocity < 0.001). Conclusion: The protocol was effective in approximately half of the MdDS patients that took part in the study, with no placebo effect recorded. The Motion-Triggered group responded better to treatment than the Spontaneous group. In addition to this, this study indicates that the greatest postural changes occur within the first 3 days of treatment, suggesting that a shorter protocol is possible. Overall, these findings support what was previously observed in Dai's studies, that optokinetic stimulation can reduce and ease self-motion perception in those with MdDS. Thus, validating the reproducibility of this protocol, suggesting that a consistent and uncomplicated implementation across treatment centers is possible.
    Keywords:  Mal de debarquement syndrome; MdDS; optokinetic stimulation; placebo; spontaneous and motion triggered MdDS
  2. Dtsch Arztebl Int. 2018 Oct 12. pii: arztebl.2018.0687. [Epub ahead of print]115(41): 687-696
    Koch A, Cascorbi I, Westhofen M, Dafotakis M, Klapa S, Kuhtz-Buschbeck JP.
      BACKGROUND: Seasickness and travel sickness are classic types of motion illness. Modern simulation systems and virtual reality representations can also induce comparable symptoms. Such manifestations can be alleviated or prevented by various measures.METHODS: This review is based on pertinent publications retrieved by a PubMed search, with special attention to clinical trials and review articles.
    RESULTS: Individuals vary in their susceptibility to autonomic symptoms, ranging from fatigue to massive vomiting, induced by passive movement at relatively low frequencies (0.2 to 0.4 Hz) in situations without any visual reference to the horizontal plane. Younger persons and women are considered more susceptible, and twin studies have revealed a genetic component as well. The various types of motion sickness are adequately explained by the intersensory conflict model, incorporating the vestibular, visual, and proprioceptive systems and extended to include consideration of postural instability and asymmetry of the otolith organs. Scopolamine and H1-antihistamines, such as dimenhydrinate and cinnarizine, can be used as pharmacotherapy. The symptoms can also be alleviated by habituation through long exposure or by the diminution of vestibular stimuli.
    CONCLUSION: The various types of motion sickness can be treated with general measures to lessen the intersensory conflict, behavioral changes, and drugs.
  3. BMJ Case Rep. 2018 Nov 05. pii: bcr-2018-226698. [Epub ahead of print]2018
    Paxman E, Stilling J, Mercier L, Debert CT.
      A 61-year-old man sustained a mild traumatic brain injury (mTBI) following a pedestrian versus vehicle traffic accident. Post injury, he began to experience symptoms including light-headedness, spatial disorientation, nausea, fatigue and prominent dizziness brought on by postural change, physical activity or eye movements. Symptoms of dizziness persisted for over 5 years, despite numerous extensive and rigorous vestibular and vision therapy regimens. All investigations suggested normal peripheral and central vestibular functioning. The patient underwent 10 sessions of repetitive transcranial magnetic stimulation (rTMS) treatment, with stimulation of the left dorsolateral prefrontal cortex at 70% of resting motor threshold and a frequency of 10 Hz. Dizziness symptom severity and frequency were reduced by greater than 50% at 3 months post treatment, with a clinically significant reduction of dizziness disability from 40 to 21 points on the Dizziness Handicap Inventory. We propose rTMS as a safe, effective and cost-effective treatment option for patients who experience persistent post-traumatic dizziness secondary to mTBI.
    Keywords:  ear, nose and throat/otolaryngology; neurological injury; rehabilitation medicine
  4. J Neurosci. 2018 Nov 09. pii: 1350-18. [Epub ahead of print]
    Chen ZP, Zhang XY, Peng SY, Yang ZQ, Wang YB, Zhang YX, Chen X, Wang JJ, Zhu JN.
      Vestibular compensation is responsible for the spontaneous recovery of postural, locomotor and oculomotor dysfunctions in patients with peripheral vestibular lesion or posterior circulation stroke. Mechanism investigation of vestibular compensation is of great importance in both facilitating recovery of vestibular function and understanding the post-lesion functional plasticity in the adult central nervous system. Here, we report that postsynaptic histamine H1 receptor contributes greatly to facilitating vestibular compensation. The expression of H1 receptor is restrictedly increased in the ipsilesional rather than contralesional GABAergic projection neurons in the medial vestibular nucleus (MVN), one of the most important centers for vestibular compensation, in unilateral labyrinthectomized male rats. Furthermore, H1 receptor mediates an asymmetric excitation of the commissural GABAergic but not glutamatergic neurons in the ipsilesional MVN, which may help to rebalance bilateral vestibular systems and promote vestibular compensation. Selective blockage of H1 receptor in the MVN significantly retards the recovery of both static and dynamic vestibular symptoms following unilateral labyrinthectomy, and remarkably attenuates the facilitation of betahistine, whose effect has traditionally been attributed to its antagonistic action on the presynaptic H3 receptor, on vestibular compensation. These results reveal a previously unknown role for histamine H1 receptor in vestibular compensation and amelioration of vestibular motor deficits, as well as an involvement of H1 receptor in potential therapeutic effects of betahistine. The findings provide not only a new insight into the post-lesion neuronal circuit plasticity and functional recovery in the central nervous system, but also a novel potential therapeutic target for vestibular disorders.Significance statementVestibular disorders manifest postural imbalance, nystagmus and vertigo. Vestibular compensation is critical for facilitating recovery from vestibular disorders, and of great importance in understanding the post-lesion functional plasticity in the adult central nervous system. Here, we show that postsynaptic H1 receptor in the medial vestibular nucleus (MVN) contributes greatly to the recovery of both static and dynamic symptoms following unilateral vestibular lesion. H1 receptor selectively mediates the asymmetric activation of commissural inhibitory system in the ipsilesional MVN and actively promotes vestibular compensation. The findings provide not only a new insight into the post-lesion neuronal circuit plasticity and functional recovery of central nervous system, but also a novel potential therapeutic target for promoting vestibular compensation and ameliorating vestibular disorders.