A Potential Missing Link Managing Mal De Debarquement Syndrome

Mal De Debarquement Syndrome can be extremely debilitating. I have enjoyed hearing Dr. Djalilian speak in the International Vestibular Diploma Course and wanted to dig a little deeper into some of his research. Here is an abstract I wrote based on his research on MdDS. I included some helpful links below as well.

Ghavami, Y., Haidar, Y. M., Ziai, K. N., Moshtaghi, O., Bhatt, J., Lin, H. W., & Djalilian, H. R. (2017). Management of mal de debarquement syndrome as vestibular migraines. The Laryngoscope, 127(7), 1670–1675. 

Purpose: 

Mal De Debarquement Syndrome (MdDS) is a sense of continuous movement, often described as rocking, that continues for weeks, months, or years after being on a ship, plane, train, or other prolonged continuous movement-related activity.  Unfortunately, traditional vestibular rehab can sometimes be unsuccessful at providing relief.  Nortriptyline and other migraine prophylactic medications have been reported to help suffering individuals find relief.  The purpose of this study was to investigate whether or not migraine prophylaxis would help decrease dizziness and improve quality of life in individuals suffering from MdDS.

Methods:

Clients battling dizziness and balance disorders, who presented to the researcher's tertiary neurotology clinic, were triaged into various diagnostic categories.  32 total patients met the MdDS criterion and were enrolled in their study.  15 clients were treated with education on migraine lifestyle changes and participated in the researcher's prescription-based migraine protocol.  This protocol included the following possible drugs individually or combined in various groups: Nortriptyline, Verapamil, and/or Topiramate.  Nortriptyline was the most common drug prescribed.  The trial cohort was compared with 17 past patients treated with vestibular rehabilitation and physical therapy (control group).

Results:

73% of the trial cohort had a large improvement reported using a visual analog scale (VAS).  A statistically significant difference was found in some quality of life (QOL) measures using a pre/post-treatment QOL survey.  There was minimal to no change in VAS or QOL in the control group.

Conclusion:

This study reinforces the hypothesis that MdDS will respond well to migraine prevention-based lifestyle change education combined with a special migraine prophylactic drug management protocol.  

Relevance to Physical Therapy:

Physical therapists helping clients battle MdDS should be aware that the potential cause for failure to compensate may be migrainous.  Therefore, positive treatment outcomes may be more likely when migraine prevention-based lifestyle changes such as diet, sleep hygiene, and stress reduction education are employed in conjunction with the migraine prophylactic protocol described in this study.  In my opinion, neck therapy and overall health and wellness programs should also be considered.  If improvement within three to six visits (usually over a period of two to three weeks) is not realized, a change in the treatment approach should be initiated.  It is not clear if this type of therapy was included in their control group.  

Links:

Original Research Article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5823515/

Dr. Djalilian (one of the authors of this article) giving an outstanding lecture on Migraine management: https://www.youtube.com/watch?v=ZpK_uId5onQ&t=4750s

The Plastic Brain and 20/20/30

Brain imaging results and function do not always correlate with one another.  For instance, I will never forget working with a four year old many years ago.  He did not want to lie down because he was dizzy.  He demonstrated typical BPPV nystagmus, but I knew this was not likely for his age.  His positional vertigo went away in about three to four days.  He went on to have fevers and periods of ataxia that would resolve.  His speech and cognition would sometimes seem sluggish and delayed.  After months of testing, he was found to have a very rare spinal cord and brain tumor that affected his cerebral spinal fluid.  He was eventually diagnosed with a low grade glioma that is classified as a juvenile pilocytic astrocytoma. He had two cystic tumors removed- one from the cerebellum and one from the spine.  

We realized that he was amazing at compensating.  His brain was phenomenally plastic.   Imaging would reveal significant hydrocephalus with his tumors.  However, through our time in trying to figure out what was wrong, his symptoms would improve and he would “return to normal.”  We realized that his brain would compensate.  His tumors and hydrocephalus developed slowly enough that his brain would adapt.

While imaging can sometimes reveal a problem that our body can adapt to hide, sometimes our body can reveal a problem that imaging is not sensitive enough to find.  This occurs with acute brainstem strokes.  When it comes to brainstem strokes, remember 20/20/30.

I had a 45 year old gentleman who had been to the ED because of vertigo.  His CT was normal and he was told he had BPPV and referred to me.  I saw him five days later.  He described his spells as untriggered and lasting 15-30 minutes.  Spells seemed to be about two to three days apart meaning he could go a few days with no dizziness at all.  While he sat in my exam room, he said, “here it comes.”   He proceeded to have an attack of spinning and vomiting.  As I looked in his eyes, I noted direction changing nystagmus.  Since this was central sign and his history was not at all consistent with BPPV, I sent him to the ED where he progressed to have a cerebellar stroke.  He was having TIAs that the CT scans were not sensitive enough to find.  

What occurred to this gentleman was not uncommon.  20% of strokes occur in the cerebellum/brainstem and only have isolated vertigo as symptoms 20% of the time.  As a result, these kinds of strokes are missed about 30% of the time(1).   One major reason is that CT scans have 16% sensitivity (2) and diffusion weighted imaging-magnetic resonance imaging performed within 24 hours from symptom onset miss about 20% of acute posterior fossa infarctions(3).  The good news is that there is an alternative and we can help these individuals find help faster using the HINTS+ battery of  bedside tests.  A positive HINTS+ test exam of a client in Acute Vestibular Syndrome (Head impulse normal bilaterally, central appearing direction changing nystagmus, a skew deviation, and new hearing loss), is reported to suggest central pathology and have 99.9% sensitivity and 97% specificity in detecting posterior circulation infarcts(4).  I will never forget 20/20/30.

References

1. Venhovens J, Meulstee J, Verhagen WI. Acute vestibular syndrome: a critical review and diagnostic algorithm concerning the clinical differentiation of peripheral versus central aetiologies in the emergency department. J Neurol. 2016;263(11):2151-2157.
2. Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009;40(11):3504-3510.
3. Newman-Toker DE. Missed stroke in acute vertigo and dizziness: It is time for action, not debate. Ann Neurol. 2016;79(1):27-31.
4. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med. 2013;20(10):986-996.

Diagnostic Imaging and VNGs in the Dizzy World

I am currently taking a class on diagnostic imaging.  I am going to post my hypothetical response to a patient for our discussion group here, but before I do, I want to underscore the value of a few key elements.  

#1.  When it comes to diagnosing dizziness, I want to emphasize the big three.  When it comes to helping clients figure out why they are dizzy, I always say "The Big Three is Key."  The big three are triggers, timing, and nystagmus.  Add in whether or not hearing loss is present, and we are really moving in the right direction for helping confirm the cause of dizziness.  Never underestimate the value of a high quality thorough history and bedside exam.  Also, if a client is having spells that are not present at the time of the clinical visit, have them video their eyes during an attack!  So much valuable information can be gained by doing so!  

Here is a link to the American College of Radiology's recommendations regarding when to order imaging for people who have sudden onset of dizziness and/or hearing loss.  https://acsearch.acr.org/docs/69488/Narrative/

#2.  "Normal" VNGs completed on individuals who are asymptomatic only provide insight regarding performance of the inner ear and brain at the time the VNG was performed.  Using a cell phone to record eye movements during spells should be encouraged when VNG results do not provide answers regarding why a client is dizzy.  Caution should be exercised before telling clients they have no inner ear or brain problems simply because the VNG was "normal" in the absence of symptoms.

#3.  Abnormal results on MRIs may or may not have meaning.  Please see my hypothetical response below addressed to an individual with low back pain:

You are seeing a 49 yo patient with a 4 week history of low back pain and they are very upset because their physician did not order an MRI.  Outline a potential response to this patient.  Can you imagine a scenario where the patient's frustration is justified?

 

I understand your concern for wanting an MRI.  However, according to the American College of Radiology guidelines, an MRI is not warranted right now because you have no red flags.  If you had a traumatic onset, a history of spinal surgery, osteoporosis, a history of cancer, suspicion of cancer, infection,  weakness or changes in your bowel/bladder, your Physician would probably be more likely to order an MRI and your frustration would certainly warrant a phone call from myself to your Physician.  These recommendations are based upon studies of thousands of different individuals combined with collaboration of experts with years of experience.  Also, please consider a study done in 2015.  The study was done on 1211 asymptomatic subjects.  87.5% had significant disc bulging, but no symptoms!(1).  Another study on 67 individuals found about ⅓ of asymptomatic individuals to have abnormal findings (2).  These individuals were surveyed over a seven year period and the abnormal findings were unable to predict which individuals would develop pain (3).  What matters most is our clinical findings at this time.   For now, I believe we can help your back pain with therapy.    

1.    Nakashima H, Yukawa Y, Suda K, Yamagata M, Ueta T, Kato F. Abnormal findings on magnetic resonance images of the cervical spines in 1211 asymptomatic subjects. Spine (Phila Pa 1976). 2015;40(6):392-398.

2.    Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am 1990;72:403- 8

3.    Borenstein DG, O'Mara JW, Jr., Boden SD, Lauerman WC, Jacobson A, Platenberg C et al. The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects : a seven-year follow-up study. J Bone Joint Surg Am 2001;83-A:1306-11.

 

Finding Answers Sometimes Takes Time...Especially if We Forget Our Roots

Reading the articles this week and watching the videos for class have reminded me of a very meaningful discussion I had with a referring ENT who had been practicing medicine 50 years.  During our conversation, I asked him what had changed the most during his time since his practice began in the 1950s.  He shared two major patterns he had identified. 

First, he stated that MRIs and CT scans had created a belief in our culture that many people could and should be diagnosed very quickly.  He explained that many people do not understand that finding a diagnosis to their problem sometimes takes time for the symptoms and disease to evolve.  He stated MRIs and CT scans had created unrealistic expectations from our patients and had also changed practice patterns of many healthcare providers.  Interestingly, Chou et al shared how these expectations can sometimes cause lack of trust in their healthcare providers if imaging is not performed. (1)  

Another great lesson my ENT friend shared is that many healthcare providers had lost the art of taking a strong history and performing a thorough bedside exam.  He stated some providers had placed too much confidence in imaging.  He stated that too many were ordering special tests instead of listening to their patients and holding true to the roots of medicine.  He explained that many had abandoned a thorough bedside exam in exchange for referring patients for more expensive testing.  

I have reflected on his observations many times over the years.  My heart breaks when I hear my clients detail the months of extensive tests and referrals they have endured.  In the context of back pain, Chou et al claim that, “routine imaging does not seem to improve clinical outcomes and exposes patients to unnecessary harms.  Imaging can lead to additional tests, follow-up, and referrals and may result in an invasive procedure of limited or questionable benefit.” (1)   

At times, I have found the dizzy world to be similar.   Many patients demand CT scans or MRIs.  They spend weeks, months, and even years going from test to test and specialist to specialist.  I have patients with dizziness spend thousands of dollars on CT scans, MRIs, VNGs, etc.  They see specialist after specialist and take months to find answers regarding why they are dizzy.  By the time they see me, they are so frustrated and have lost hope.  They lack hope in healthcare and they lack hope they will improve. In addition, they may often be in the vicious cycle of dizziness that involves avoidance, disuse, and fear that makes their problems worse.   I believe we, as passionate and knowledgeable healthcare providers, can change this paradigm through teamwork.  

Teams of healthcare providers sharing the same high quality education about the reason for symptoms followed by ways to address those symptoms and improve quality of life helps greatly.  My best results are obtained when the referring Physician and I are speaking the same language regarding the diagnosis and plan to improve.  Physicians who prepare patients for success by completing a thorough history and exam followed by a confident referral my way has lead to great outcomes.  I am often able to complete basic bedside tests and a highly sensitive/specific history that helps.  Spending time with the patient and learning how to speak their language provides them with the aha moment they are seeking.  I can often see the stress relieved from their shoulders as explanations are given through providing high quality dizziness neuroscience education.  

It is not  unreasonable for our patients to expect a quick and accurate diagnosis.  However, somehow we have to shift their confidence away from machine based diagnostics toward trusting the expertise of their healthcare provider(s).   Machine based results are often misleading.  For instance, “most lumbar imaging abnormalities are common in persons without low back pain and are only loosely associated with back symptoms.” (1)  

The bottom line is that people want to know why they are in pain or why they are dizzy.   People in general love machines and they trust those kinds of results.  However, these machines are often not able to provide the proper answers our clients seek.   We have to use our bedside exam skills, research articles available, and take the time required to provide high quality education in a way they can understand, believe, and then change their lives by changing their perspective.

1. Chou R, Qaseem A, Owens DK, Shekelle P; Clinical Guidelines Committee of the American College of Physicians. Diagnostic imaging for low back pain: advice for high-value health care from the American College of Physicians [published correction appears in Ann Intern Med. 2012 Jan 3;156(1 Pt 1):71]. Ann Intern Med. 2011;154(3):181-189.

Red Light Dizziness and Red Light Pain. So Much In Common. So Much to Learn From One Another!

Red Light Dizziness and Green Light Dizziness

Red Light Pain and Green Light Pain

Well.  Here I go again.  I can't help but relate all of these concepts we are learning about pain to the dizzy world.  I love reading these articles and everyone's discussion board entries and listening to the lectures because they are helping me connect the dots from those battling dizziness with those battling pain.  For instance, after treating thousands of clients with dizziness for over 20 years, I have learned the following slide to be very true for so many of my patients.  A dizziness trigger can be any dizziness related problem (often BPPV, Migraine, or Neuritis/Labyrinthitis) or thought (sometimes the idea that one could fall or one could become dizzy) to trigger sensory reweighing.  Sensory reweighing is a complex nervous system process that turns sensory input from the vestibular system down (or up) and often leads to the vicious cycle of dizziness you see below:

My role as a dizzy therapist is to get rid of the dizziness trigger as quickly as possible.  This might mean fixing the BPPV, promoting vestibular adaptation for neuritis, or teaching how to prevent Migraines.  These triggers often create intense spinning that require a special kind of treatment.  I call this type of spinning: "Red Light Dizziness."   When individuals have red light dizziness they need to stop, call me, do a maneuver, take a medication, etc.  However, once the red light dizziness is gone, they need to move normally.  This leads to how to break the vicious cycle of dizziness.  They need to adapt a "bring it on baby" mentality.  They welcome dizziness as an opportunity to improve and promote healing.  I call this stage "green light dizziness."  Green light means go.  The feeling that you could become dizzy is not a sign you will become dizzy.  I spend a lot of time educating individuals because it calms their nervous systems and promotes improved healing.

My point is that all of our readings and discussions have given me confidence that I can use a similar approach with my clients with pain.  I need to try to discover the cause of their pain.  I need to stabilize the cause and make sure it is not dangerous.  Once that is done, I need to help them grow and learn to break the vicious cycle they are likely battling through.  The complex nervous system involvement in the dizzy world sounds extremely similar to the world of pain.  Using words like "red light pain" and "green light pain" might help them learn to welcome certain types of pain as an opportunity to get stronger while other types of pain may indicate something needs to be adapted or changed.  I need to teach them that the feeling like they could have pain is not the same as having pain. 

1. Butera KA, Fox EJ, George SZ. Toward a Transformed Understanding: From Pain and Movement to Pain With Movement. Phys Ther. 2016 Oct;96(10):1503-1507. Butera_pain and movement_PTJ.pdf
   
2. Costigan M, Scholz J, Wolf CJ. Neuropathic Pain: A maladaptive response of the nervous system to damage. Annual Review Neuroscience, 2009;32:1-32. (not required; useful if this content is new to you) Costigan_Neuropathic pain_Annu Rev Neurosci.pdf
   
3. Bushnell CM, Ceko M, Low LA. Cognitive and emotional control of pain and its disruption in chronic pain. Nat Rev Neurosci 2013;14(7):502-511. Bushnell_emoational cognitive control pain_Nat Rev neurosci.pdf
   
4. Kerstman E, Ahn S, Battu S, Tariq S, Grabois M. Neuropathic Pain Handbook of Clinical Neurology 2013;110:176-87. (all should read this) Kerstman_Neuropathic pain.pdf
   
5. Pergolizzi J et al. Commentary: The development of chronic pain: physiological CHANGE necessitates a multidisciplinary approach to treatment. Current Medical Research & Opinion 2013;29(9):1127-1135. Pergolizzi_Chronic pain_CMRO.pdf
   

What Do the Vestibular Nerve and Pain Nerve Fiber's Have In Common?

Scarpa's Ganglion Compared to Dorsal Root Ganglion?

In the peripheral vestibular system, Scarpa's Ganglion have a baseline firing rate of 100 spikes/second making the objective findings from a lesion possible.  Both Scarpa's Ganglion oppose one another (there is one on the right and left).  They play tug of war.  When one becomes irritated, it pulls harder than the other and when one becomes inhibited, it "let's go" of the rope.  This is the mechanism behind the fast and slow phases of nystagmus.

The question I have is do the ganglion in pain fibers have a baseline firing rate that would allow us to somehow find an objective signal that would allow us to "see" pain? 
After a quick PubMed search, I found a quote by Krame's that has spiked my curiosity into this matter: "In the not-too-distant past, the dorsal root ganglion (DRG) was portrayed as a passive neural structure without involvement in the development or maintenance of chronic neuropathic pain (NP). The DRG was thought of as a structure that merely "supported" physiologic communication between the peripheral nervous system (PNS) and the central nervous system (CNS). Newer scientific information regarding the anatomic and physiologic changes that occur within the DRG as a result of environmental pressures has dispelled this concept and suggests that the DRG is an active participant in the development of NP. This new information, along with new clinical data showing that stimulation of the DRG reduces intensity of pain, suggests that the DRG can be a robust target for neuromodulation therapies."¹

Perhaps a decrease in pain following stimulation to the dorsal root ganglion is as objective as we can get?


Krames ES. The dorsal root ganglion in chronic pain and as a target for neuromodulation: a review. Neuromodulation. 2015;18(1):24‐32. doi:10.1111/ner.12247

What Can the Pain Management World Learn from the Dizzy Management World?

The following is an entry I wrote for my discussion board in tDPT school today. The idea of comparing these two worlds thrills me!

Hypofunctions and Hyperfunctions:  The Dizzy World’s Contribution to the Invisible World of Pain. 

Since I am a dizzy therapist, I can’t help but love comparing this information with my specialty.  In Shmid’s article, the authors state,  “symptoms and signs in neuropathies can be classified as gain or loss of function. Gain of function, such as paraesthesia, spontaneous pain, hyperalgesia and allodynia, reflects abnormal excitability or reduced inhibition in the nervous system. Loss of function, such as hypoesthesia or anaesthesia, indicates reduced impulse conduction along the nervous system (Woolf, 2004).”1  Woolf et al elaborate by stating, “Peripheral neuropathic pain (Links to an external site.), that clinical pain syndrome associated with lesions to the peripheral nervous system (Links to an external site.), is characterized by positive and negative symptoms. Positive symptoms include spontaneous pain, paresthesia (Links to an external site.) and dysthesia, as well as a pain evoked by normally innocuous stimuli (allodynia) and an exaggerated or prolonged pain to noxious stimuli (hyperalgesia/hyperpathia). The negative symptoms essentially reflect loss of sensation due to axon/neuron loss, the positive symptoms reflect abnormal excitability of the nervous system.”2  In summary, Shmid’s terminology of “gain of function” can be compared to Woolf’s “positive symptoms” and “loss of function” can be compared to “negative symptoms.”  What is thrilling, is the comparison of this terminology with both subjective and objective findings in the world of dizziness.

Comparison of this terminology is remarkably accurate when related to the vestibular world.  More shocking, though, is the objective insight the dizzy world provides for the therapist trying to understand the impact of pain on our nervous system.   Indeed, what I have learned from the vestibular world is mind blowing when applied to the pain world and this terminology.  

First, it is helpful to understand that peripheral vestibular problems can be organized into two major categories: Hypofunctions and Hyperfunctions.  Causes of vestibular hyopfunctions include, and are not limited to: Neuritis, Labyrinthitis, Chronic Meniere’s, Dysequilibrium of Aging, Ischemia, etc and vestibular hyperfunctions: BPPV and Acute Meniere’s.  It is interesting that dizzy subjective symptoms are very similar to the pain subjective symptoms in hypo and hyperfunctions.  For instance, a few of the sensory problems caused by vestibular hypofunctions include: delay, off, things have to catch up, and off balance.  In addition, sensory problems caused by hyperfunctions include: intense spinning, nausea, vomiting, and astounding fear/avoidance.  Both categories of vestibular problems compare nicely with the “negative” and “positive” symptoms described by Woolf et al.2  

More astounding, though, is the fact that the dizzy objective findings can be seen and correlated with the subjective symptoms.   Vestibular hyopfunctions and vestibular hyperfunctions cause obvious objective signs that, when compared to the pain world, might give health care providers treating pain insight into an invisible world.  When a client has a hypofunction they will have nystagmus that beats away from the side of the lesion.  When a client has a hyperfunction, they will have nystagmus that beats toward the side of the lesion.  The nystagmus is often symptomatic and, in the case of BPPV, one can often tell the client what they are feeling without them having to say anything.  

These objective findings in the vestibular world help provide credibility and proof that categorizing peripheral nerve injuries as gain of function and loss of function can be compared to hyperfunction and hypofunction in the vestibular world.  The objective findings in the dizzy world can provide confirmation of the reality of the science of symptoms relating to pain.  

References

1. Schmid et al. Reappraising entrapment neuropathies - Mechanism, diagnosis, and management.  Man Ther 2013. 449-457.
2. Woolf CJ. Dissecting out mechanisms responsible for peripheral neuropathic pain: implications for diagnosis and therapy. Life Sci. 2004;74(21):2605‐2610.