Case Study

Funct Neurol Rehabil Ergon 2013;3(1):93-107

ISSN: 2156-941X © Nova Science Publishers, Inc.


EAR INSUFFLATION AS A NOVEL THERAPY WHICH PRODUCES RAPID RELIEF OF MIGRAINE HEADACHE - CASE SERIES
David B. Sullivan* 

ABSTRACT

Background: The many varieties of migraine headaches and their associated neurological dysfunctions represent a significant source of pain and suffering to our society. For many, migraine headaches are a chronic source of pain and significantly impact one’s quality of life. With the aim of reducing the impact of chronic neurological illness, a functional approach to neurorehabilitation has emerged as a paradigm shift within the context of neurological health care. This growing body of knowledge, related to assessing and optimizing the function of the nervous system, serves as the basis for seeking effective non-pharmaceutical and non-surgical therapeutic strategies for the treatment of chronic neurological disease.

Objective: The purpose of the current study was to investigate the effectiveness of pneumatic insufflation of the ear in alleviating migraine symptoms during an acute attack.

Design: Thirteen patients were recruited to test this experimental procedure. Some were initially given a sham treatment in order to confirm response/non-response to the procedure.

Results: The results indicate that nine subjects experienced rapid, complete or near-complete relief from their headache, three subjects experienced only moderate relief and one subject demonstrated no response. The implications of this novel therapy are vast, not only as a potential treatment option for migraine, but as validation of the use of specific afferent activation as a way to modulate neurological functionality. This is the first instance within the neurological literature that ear insufflation has been documented as an effective intervention in the elimination of migraine symptomatology.

Keywords: Migraine, Headache, Trigeminal Nerve, Auriculotemporal Nerve, Ear Insufflation, Neurorehabilitation, Clinical Application

 

INTRODUCTION

The potential degree of human suffering and effects on quality of life cannot be overstated in the case of chronic migraine. This affliction can negatively impact nearly every facet of one’s family, home and work life, relationships, school, leisure and social time. Beyond the individual burden of this illness is the significant strain which falls upon the healthcare delivery system, employers and our society at large related to costs associated with chronic migraine, both direct and indirect [1].

The variants of migraine headaches and their concomitant symptoms such as nausea, aura, photophobia, dysesthesias and dysequilibrium represent a significant burden to the population at large. Epidemiological studies indicate that approximately 18% of the United States’ female population, and 6% of men, experience frequent migraines and 2% of the general population suffer with chronic migraine headaches [2]. The significance of these statistics cannot be understated. Insight, understanding and wisdom on the part of the skilled clinician would make it very clear to both patient and community that migraine headaches are not just exacerbated tension-type headache. Migraines are in fact a neurological disease. Additionally, and speaking to the severity of this situation, persons suffering with chronic migraines or other headaches of similar severity and disability are at a significantly greater risk for suicide attempt [3]. With this understanding, it is prudent for clinicians and researchers to continue searching for effective therapies and applications in order to reduce this burden of suffering on our society.

Standard pharmaceutical therapies for migraine headaches are generally prescribed for two different purposes: pain relievers or pain preventatives. The various agents which fall under these two broad categories exhibit a wide range of effectiveness and also incur varying degrees of side effects [4,5]. From the perspective of economics, the expense of these medications, which amounts to approximately $ 1.5 billion per year and $160 per triptan prescription, can be a major source of financial burden on the consumer [6]. Even more troubling are the economic and physical realities when these front line therapies fail to achieve significant relief. Advanced interventions such as botulinum toxin injections, nerve blockades, neurosurgical alterations and implanted electrical stimulators can significantly increase costs associated with treatment, while subjecting patients to sometimes permanent changes in their anatomy and physiology, with no guarantee of complete or permanent symptomatic relief [7-11].

With a very different approach to therapy, there is a burgeoning field of understanding and applications within the neurosciences, which seeks to affect positive physiological changes in the neuraxis through non -pharmaceutical and non -surgical applications [12]. This field of ‘functional neurology’ has, at its core, the understanding that the human nervous system is a receptor driven system and can be activated and stimulated in specific ways to produce adaptive, long-term changes through the process of neuroplasticity [13]. This approach to neurorehabilitation utilizes, heavily but not exclusively, various forms and patterns of receptor activation in order to promote positive neurophysiological adaptations within the brain, brainstem and spinal cord [14,15] which then promote optimized physiological function of associated tissues, organs and systems. It is within this paradigm that the current investigation was carried out.

To date, there have been a variety of studies which have demonstrated that beneficial cortical excitation can be achieved through various stimuli via cranial nerves and concomitant brainstem integration [16- 22]. Central pain states, balance disorders and more have been shown to be positively affected by this type of approach. Typically performed with the application of caloric irrigation, both cold and warm, galvanic electrical stimulation, oculomotor activities or head movements, these studies have greatly advanced the understanding of how activation of the related pathways can alter symptomatology by way of altering cortical functionality [23-36]. The author predicts that other forms of somatomotor and/or somatosensory excitations can be likewise successful in producing significant and reliable symptomatic changes, in this case - trigeminal excitation via pneumatic insufflation at the external auditory meatus. Our task was to investigate the effectiveness of this simple, non-invasive, low-cost and readily available bedside therapy. 

METHODS

For the current investigation, we recruited thirteen patients who were in the midst of a migraine attack, in order to investigate the effectiveness of pneumatic ear insufflation on the reduction of pain levels. Each subject was obtained through referral from local medical clinics and advertisement, and all but one participant had a documented history of migraine headaches. Diagnosis was re-confirmed at the time of experimentation. The current study was conducted in accordance with the ethical standards set forth in the Helsinki Declaration of 1975.

Each patient was informed as to what the current investigation would entail and what they might perceive during the treatment. This discussion did not include what they might potentially experience in terms of symptomatic change, but centered around the procedure itself. After discussing the risks of this therapeutic trial, each patient gave informed consent to proceed.

Materials and equipment used for the current investigation consisted of a diagnostic pneumatic otoscope, fitted with Welch Allyn Reusable Ear Specula #24237 and Welch Allyn Insufflator Bulb #21504.

Primarily for purposes of patient comfort and ease of application, each patient was placed in a supine position with the head slightly elevated. They were allowed to remain in this position for roughly three minutes, in order to acclimate to the supine position, lighting and environmental conditions. They were asked to remain eyes-open for the duration of the investigation. Each patient was asked to rate their level of pain at the onset of treatment, after each subsequent application, and at the completion of the procedure and at 30 minutes, 4 hours and 24 hours post-treatment. Pain was rated with a visual analog scale (VAS) with zero (0) representing no pain at all, and ten (10) representing the highest possible level of pain (Figure 2).

In order to validate the difference between actual insufflation and a sham treatment, some patients were first administered successive 30-second rounds of having the otoscope with insufflation speculum placed in the ear canal with no pneumatic pressure applied. Multiple rounds of this sham procedure were applied. The sham application was discontinued if there was no change in symptoms for three consecutive rounds.


Figure 2. Patient visual analog pain scale response after each round of treatment.

The experimental ear insufflation procedures were administered with a 7.0 mm diagnostic reusable speculum in roughly 30-second intervals to the ear on the side of the head that was most symptomatic. Multiple rounds of pneumatic insufflation were applied. The pressure applied was mild; enough to produce observable deflection of the tympanic membrane, but not so much as to cause discomfort with either positive or negative pressure. A pulsatile pressure was applied at approximately 2 Hz. If the patient reported continued and positive response with each application, treatment was continued in order to determine how much symptomatic improvement could be obtained. Treatment application was discontinued when there was no change in symptoms for three consecutive rounds.

Additionally, experimental application was discontinued before 30 seconds if the patient noted any sign of autonomic changes including, but not limited too, flushing of the face, increased salivation, lacrimation or hyperventilation. Application was resumed only after any of these signs returned to normal limits.

RESULTS

Patient number 1 was a right-handed, 38- year-old female. Her pertinent history of migraine included 10 years of severe migraines occurring around 20 days per month. Previous MRI evaluation revealed early degenerative disc changes at C5-6 and no abnormalities detected in the brain. Her current pharmaceutical regimen pertaining to migraine consisted of sumatriptan 100 mg at the onset of symptoms. She reported that if she would fail to take sumatriptan in the earliest stages of her headache, the pain would quickly escalate and become refractory to any interventions, typically leading to emergency medical care. Pre-treatment neurologic exam revealed light and sound sensitivity as well as tactile allodynia on the left side of her face and neck. She also reported having aura and nausea. On questioning, she stated that she had not taken any prescription drugs or other over-the-counter remedies within the last eight hours for the current headache. Her pre-treatment rating of pain on a visual analog scale was 5/10.

 She was administered the sham procedure first. The patient reported VAS scores of 5 before and 5 after, so the sham procedure was discontinued. She was then administered the experimental treatment. Over successive rounds of treatment, her VAS pertaining to face/head pain was 5, 5, 5, 4, 4, 3, 2 and 1. VAS scores pertaining to neck pain were 5, 5, 5, 5, 5, 5, 4, 3, 3 and 3. Total treatment time was approximately 12 minutes. Post-treatment neurological exam revealed the absence of light and sound sensitivity and she reported that her nausea had resolved. At thirty minutes after completion, her VAS was 0 (face) and 1 (neck). Four hours post-treatment, she reported a slight recurrence of pain; 1 (face) and 2 (neck). At 24 hours post-treatment, she reported a VAS of 1 (face) and 2 (neck). There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 2 was a right-handed, 38-year-old female. Her pertinent history of migraine included 25 years of almost daily migraine with aura. Her previous treatments for headaches included occipital nerve stimulator, occipital nerve blocks and botulinum toxin injections. Previous imaging of the brain was negative. Pre-treatment neurologic exam revealed light sensitivity and tactile allodynia around the left occipital and temporal areas. She reported aura, flashes/floaters and smell sensitivity. Her current pharmaceutical regimen pertaining to migraine included over-the-counter medications, SSRIs and dopamine reuptake inhibitors. On questioning, she stated that she had not taken any prescription drugs or other over-the-counter medications within the last eight hours for this current headache. Her pre-treatment rating of pain on a visual analog scale was 6/10.

 She was administered the experimental procedure first. Over successive rounds of treatment, her VAS was 5, 4, 3, 2, 1.5, 1 and 0. Total treatment time was approximately 12 minutes. At thirty minutes after completion, her VAS scores were 5/10 and was 4/10 at 4 hours and 4/10 at 24 hours. Post-treatment neurological exam revealed the absence of light sensitivity and tactile allodynia. She reported that her aura had completely resolved as well. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 3 was a right-handed, 33-year-old female. Her previous history of migraine included 17 years of recurrent migraine of moderate to severe intensity. She denied using triptans or having any surgical interventions for headache. MRI of the head was unremarkable. The current headache was encompassing the left eye and frontal area, and had a sharp, throbbing nature. Light touch in that area provoked a pain response. She reported aura, nausea and vomiting occasionally through the day. Her current pharmaceutical regimen pertaining to migraine included over-the-counter migraine medications at the onset of symptoms. On questioning, she stated that she had taken other over-the-counter medications approximately six hours previously for the current headache. Her pre-treatment rating of pain on a visual analog scale was 6/10.

 She was administered the sham procedure first. The patient reported VAS scores of 6 before and 6 after, so the sham procedure was discontinued. She was then administered the experimental treatment. Over successive rounds of treatment, her VAS scores were 5, 2, 1 and 0. Total treatment time was approximately 6 minutes. At thirty minutes after completion, her VAS was 5/10 and was 4/10 at 4 hours and 4/10 at 24 hours. Post-treatment neurological exam revealed the absence of light sensitivity and tactile allodynia. She reported that her aura and nausea had completely resolved as well. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 4 was a right-handed, 43-year-old female. Her pertinent history of migraine included 20 years of recurrent migraine with aura occurring approximately 6 days per month. Her previous treatments for migraine included sumatriptan for prophylaxis and acute treatment. Previous imaging of the head and brain were negative. During her migraines, she would experience aura, flashes/floaters, nausea, pulsing pain, and light, sound and smell sensitivity. Her current pharmaceutical regimen pertaining to migraine included over-the-counter ibuprofen 400 mg as needed. On questioning, she stated that she had not taken any prescription drugs or other over-the-counter medications within the last eight hours for this current headache, which was present upon awakening that morning. The headache she was experiencing at the time of treatment consisted of a squeezing pressure around the temples and the base of the skull. She reported that the headache was building in intensity and would most likely develop into a full-blown migraine in the coming hours. Her pre-treatment rating of pain on a visual analog scale was 6/10.

 She was administered the experimental procedure to the left ear, because she would typically experience her migraine symptoms on the left side of her head. Over successive rounds of treatment, her VAS scores were 6, 4.5, 3, 0.5 and 0.2. Total treatment time was approximately 10 minutes. At thirty minutes after completion, her VAS was 0.5 and was 0.5 at 4 hours and 0/10 at 24 hours. She reported that there was virtually no pain upon completion of the therapy and that she felt extremely relaxed and calm. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 5 was a right -handed, 25-year-old female. She did not report a significant past history of migraine, although she presented with “the worst headache of [her] life”. She described a severe headache of 5 days duration which had a throbbing, pulsatile nature to it. She also reported dizziness, and sensitivity to light and sound associated with her headache. She stated that the headache spanned the front of her forehead, temples and the base of her head with vice-like pressure. On questioning, she stated that she had taken ibuprofen and acetaminophen earlier in the day, approximately 6 hours previously. Those medications helped to reduce her pain level from 9/10 on a verbal rating scale to her pre-treatment rating of 5/10.

 She was administered the sham procedure first. The patient reported VAS scores of 5 before and 5 after, so the sham procedure was discontinued. She was then administered the experimental treatment. Because she did not have a unilateral headache, the right ear was arbitrarily chosen as the initial treatment side. Over successive rounds of treatment, her VAS scores pertaining to right sided pain were 4, 2, and 0/10. The pain remained unchanged in the left side of her head. She was then administered the procedure to the left ear. Her pre-treatment rating of pain on the left was 5/10. Over successive rounds of treatment, her VAS scores pertaining to left sided pain were 4, 3, 1, 1 and 0.5. Total treatment time was approximately 12 minutes. There was no incidence of vertigo, nystagmus or aberrant autonomic response. Repeated attempts to ascertain her post-treatment VAS levels were unsuccessful.

Patient number 6 was a right-handed, 30-year-old female. Her pertinent history of migraine included 15 years of recurrent migraine. She experienced migraine headaches approximately 30 days per month and reported experiencing significant limitations and disability due to migraine. Her previous use of pharmacological agents for headaches included eletriptan and over the counter migraine medications. She described the current headache as severe and present for the past 24 hours. Pre-treatment neurologic exam revealed light sensitivity and tactile allodynia at the forehead and temples. She also reported dizziness and nausea. She stated that the headache had been localized to the left side of her face and head, but had evolved to encompass both sides of the forehead, temples and base of her head. On questioning, she reported that she had taken OTC migraine medication four hours previously and it had no effect. She took a second dose 30 minutes later and it brought her pain level down from a 10/10 to a 4/10. Her pre-treatment rating of pain on a verbal rating scale was 6/10 and she rated her nausea as a 7/10.

 She was administered the experimental procedure to the left ear first. Over successive rounds of treatment, her VAS scores pertaining to face/head pain were 6, 2, 0 and 0. VAS scores pertaining to nausea were 7, 0, 0 and 0. Total treatment time was approximately 6 minutes. Post-treatment neurological exam revealed the absence of light sensitivity and tactile allodynia. She reported a complete resolution of pain and nausea. At thirty minutes after completion, her VAS was 0 (pain) and 0 (nausea). Four hours post-treatment, she reported a VAS of 0/10 for both pain and nausea. At 24 hours post-treatment, she reported a VAS of 0/10 for both pain and nausea. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 7 was a right-handed, 39 -year-old female. Her history of migraine included 27 years of recurrent migraine. She experienced migraine headaches approximately 20 days per month and reported ‘severe’ impact on quality of life due to migraine headaches. Her current use of pharmacological agents for migraine included topiromate, sumatriptan and duloxetine. She had also undergone two botulinum toxin injections in the past seven months. She described the current headache as severe and present for the past 3 - 4 days. Pre-treatment neurologic exam revealed light sensitivity, slight dysarthria and tactile allodynia at the forehead and temples bilaterally. She also reported dizziness, nausea, unsteadiness with walking, left ptosis, slurred speech and sensitivity to light, sound and smell. She stated that the headache had been localized to the right side of her face and head, but had evolved to encompass both sides of the forehead, temples, top and base of her head. On questioning, she reported that she had taken sumatriptan two days previous and approximately 6 hours previously. Her pre-treatment rating of pain on a verbal rating scale was 7/10.

 She was first administered the experimental procedure to the right ear. Over successive rounds of treatment, her VAS scores pertaining to pain were 4/10, 2/10 and 1/10 with some pain remaining at the left eye. Treatment was then directed to the left ear. One 30-second round of therapy to the left ear abolished the remaining pain at the left eye. Because she noted some slight pain to palpation at the right forehead (1/10), therapy was conducted again at the right ear. One 30-second round of therapy abolished all remaining pain at the right forehead. Total treatment time was approximately 12 minutes. She reported being completely free of nausea, pain, sensitivities, and there were no detectable abnormalities in speech. She reported that her unsteady gait had returned to normal as well. At thirty minutes after completion, her VAS was 0/10 and was 1/10 at 4 hours and 3/10 at 24 hours. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 8 was a right-handed, 53-year-old female. Her history of migraine included 30 years of recurrent migraine. She experienced migraine headaches approximately 6 days per month and reported ‘moderate’ impact on quality of life due to migraine headaches. Her current use of pharmacological agents for migraine included citalopram, sumatriptan, ibuprofen and naproxen. She described the current headache as moderate and fluctuating between mild to severe over the past 7 days. The pain had become slightly worse over the previous 36 hours and she reported feeling as though the pain was starting to abate and resolve. Pre-treatment neurologic exam revealed light sensitivity and slight tactile allodynia at the left forehead. She reported nausea as a feature of the current headache and that the headache had been localized to the left side of her face and head. On questioning, she reported that she had taken sumatriptan one-day and four-days previous. Her pre-treatment rating of pain on a verbal rating scale was 5/10.

 She was first administered the experimental procedure to the left ear. Over successive rounds of treatment, her VAS scores pertaining to pain were 5/10, 4.5/10, 4.5/10 and 4.5/10. Because her pain level had been unchanged over three successive rounds, the treatment was discontinued and she was released. At thirty minutes after completion, her VAS was 6/10 and was 3/10 at 4 hours and 1/10 at 24 hours. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 9 was a right-handed, 47-year- old female. Her history of migraine included 5 years of recurrent migraine. Her primary issue was chronic daily headache of varying severity and migraine headaches approximately 4 days per month. She reported ‘moderate’ impact on quality of life due to migraines and chronic daily headaches and she could not recall any time in the previous 12 months that her pain was completely absent. Her current use of pharmacological agents for migraine included topiromate 200 mg daily, wellbutrin and over the counter migraine medication as needed. In the past four years, she had utilized physical therapy extensively and to a lesser extent, chiropractic adjustments and acupuncture, all with limited to no relief. Pre-treatment neurologic exam revealed light and sound sensitivity. There was no tactile allodynia present at the time of investigation, although she has experienced that as a feature of her migraines. She did report nausea of a moderate to intense degree. She stated that the current headache encompassed the whole head with pressure and throbbing at the forehead, temples, top and base of her head. On questioning, she reported that she had not taken any medication in the previous 24 hours. Her pre-treatment rating of pain on a verbal analog scale was 6/10 over the whole head.

 She was first administered the experimental procedure to the left ear because she would typically experience her migraine headaches on that side. Over successive rounds of treatment, her VAS scores pertaining to pain were 5/10 (bilateral), 5/10 (bilateral), 4/10 (left)-5/10 (right), 3/10 (left)-4/10 (right), 2/10 (left)-3/10 (right), 1/10 (left)- 3/10 (right) and 1/10 (left)-3/10 (right). The procedure was then applied once to the right ear which had no effect, pain levels remained at 1/10 (left)-3/10 (right). One final application was applied to the left ear and resulted in VAS of 0/10 (left)-2/10 (right). The only remaining pain was a slight irritation at the posterior aspect on the right side of her head. Total treatment time was approximately 30 minutes. Upon questioning, she reported a 90% improvement in her nausea. There was no incidence of vertigo, nystagmus or aberrant autonomic response. Repeated attempts to ascertain her post-treatment VAS levels were unsuccessful.

Patient number 10 was a right-handed, 37-year- old female. Her history of migraine included 32 years of recurrent migraine. She would experience migraine headaches approximately 12 days per month and would be generally incapacitated during those days. She reported ‘severe’ impact on quality of life due to her migraines. Her current use of pharmacological agents for migraine included tramadol 400 mg daily, duloxetine 120 mg daily, fioricet and fioricet with codeine. Her previous use of medication included prochlorperazine, hydromorphone with promethazine, and in extreme situations, she would be treated with a combination of meperidine, ketorolac and promethazine. She had also undergone occipital nerve block 3 years previously which did not have any positive effect on her pain. Past MRI examination of the head revealed no abnormalities. Pre -treatment neurologic exam revealed light and sound sensitivity. There was no tactile allodynia present at the time of investigation, although she would frequently experience that as a feature of her migraines. She did report nausea of a moderate degree. She stated that the current headache was primarily centered around the left occipital area with some radiation to the left temple and was present for the last 3 days. On questioning, she reported that she had taken a dose of fioricet approximately 5 hours previously. Her pre-treatment rating of pain on a verbal analog scale was 9/10.

 Because she was experiencing her migraine on the left side of her head, she was first administered the experimental procedure to the left ear. Over successive rounds of treatment, her VAS scores pertaining to pain were 6.5/10, 4/10 and 0/10. One final application was applied to the left ear and maintained her VAS of 0/10. She reported complete resolution of her light and sound sensitivity as well as her nausea. Total treatment time was approximately 15 minutes. At thirty minutes after completion, her VAS was 0/10 and was 0/10 at 4 hours and 0/10 at 24 hours. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 11 was a right-handed, 53-year- old female. Her history of migraine included 3 years of recurrent migraine. She would experience migraine headaches approximately 3 days per month and would be unable to perform home or work duties during those days. She reported ‘moderate’ impact on quality of life due to her migraines. Her current use of pharmacological agents for migraine included ibuprofen as needed. Due to past history of cardiac ablation and chronic cardiac disease, she declined any more advanced pharmacological treatment. Pre-treatment neurologic exam revealed light sensitivity. There was slight tactile allodynia present at the time of investigation. She did not report any nausea. She stated that the current headache had been present for approximately 20 hours and was primarily centered around the right eye and forehead. She stated that she had recently undergone a detoxification protocol which triggered the migraine event. On questioning, she reported that she had not taken any medication for the current headache. Her pre-treatment rating of pain on a verbal rating scale was 6/10.

 Because she was experiencing her migraine on the right side of her head, she was first administered the experimental procedure to the right ear. Over successive rounds of treatment, her VAS scores pertaining to pain were 3/10, 1/10, and 1/10. She reported complete resolution of her light sensitivity. Total treatment time was approximately 10 minutes. At thirty minutes after completion, her VAS was 0/10 and was 3/10 at 4 hours, 6/10 at 8 hours and 0/10 at 24 hours. There was no incidence of vertigo, nystagmus or aberrant autonomic response although she reported some tenderness at the auditory meatus.

Patient number 12 was a left-handed, 41-year-old female. Her history of migraine included 29 years of recurrent migraine. She would experience migraine headaches approximately 20 days per month and would be mostly incapacitated during those days. She reported ‘extreme’ impact on quality of life due to her migraines. Her current use of pharmacological agents for migraine included venlaxafine HCL, verapamil, and rizatriptan. She had an extensive history of medication usage including amitriptyline, butalibital/floricet, multiple triptans, nortriptyline, topiramate, cyclobenzaprine, gabapentin and propranolol. Previous MRI of the brain showed no abnormalities. Pre -treatment neurologic exam revealed light sensitivity. There was slight tactile allodynia present at the time of investigation. She did not report any nausea. She stated that the current headache had been present for approximately 7 hours and encompassed both right and left temples and forehead. She reported blurry vision, speech abnormalities and sensitivity to lights, sounds and smells. On questioning, she reported that she had not taken any medication for the current headache. Her pre-treatment rating of pain on a verbal rating scale was 6/10.

 Although she was experiencing her migraine on both sides of her head, she reported that she would typically experience more pain on the right side. She was administered the experimental procedure to the right ear. Over successive rounds of treatment, her VAS scores pertaining to pain were 5/10, 4/10, 1/10 and 0/10. She reported complete resolution of light sensitivity and blurry vision. Total treatment time was approximately 15 minutes. At thirty minutes after completion, her VAS was 0/10 and was 0/10 at 4 hours and 1/10 at 24 hours. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

Patient number 13 was a right-handed, 15-year -old female. Her history of migraine included 6 years of recurrent migraine. She would experience migraine headaches approximately 12 days per month. She reported ‘moderate’ impact on quality of life due to her migraines. Her current use of pharmacological agents for migraine included amitriptyline. Previous MRI showed no abnormalities. Pre-treatment neurologic exam was essentially normal. She reported that her headache was generally subsiding, but that there was some residual pain and mild nausea. She stated that the current headache had been present for approximately 4 days and encompassed both sides of her head. On questioning, she reported that she had taken ibuprofen approximately 6 hours previous. Her pre-treatment rating of pain on a verbal rating scale was 3/10.

 Although she was experiencing pain on both sides of her head, she reported that she would typically experience more pain on the right side. She was administered the experimental procedure to the right ear. Over successive rounds of treatment, her VAS scores pertaining to pain were 3/10, 2.5/10, and 0/10. Total treatment time was approximately 10 minutes. At thirty minutes after completion, her VAS was 0/10 and was 0/10 at 4 hours and 0/10 at 24 hours. There was no incidence of vertigo, nystagmus or aberrant autonomic response.

DISCUSSION

Migraine headaches are typically referred to as a neurovascular headache event. This term places emphasis on the understanding that migraines are not exclusively the result of vascular dysfunction, but include many other neurological processes as well [36]. Various theories have been proposed to describe the exact pathophysiology of migraine, including vascular induced or centrally-generated changes, but none have fully explained the complete spectrum of symptoms under one model [37,39]. The current study seems to lend credence to a centrally mediated pathophysiological mechanism because of the direct and immediate response upon stimulation of suprasegmental pathways. If this causative relationship between central activation/dysfunction and the symptoms of migraine is to be understood, then questions arise regarding how and why the effects of ear insufflation appear to be so promising in relieving the pain and neurologic concomitants of migraine headaches.

First, because the deflection induced on the tympanic membrane with ear insufflation does not, or should not, involve an auditory component, it would seem unlikely that the observed effects are due particularly to stimulation of the cochlear portion of cranial nerve (CN) 8. However, the basilar membrane within the cochlea will undergo mechanical displacement upon compression and rarefaction and could subsequently be activating afferent projections from hair cells along the length of the membrane [40]. The vestibular component of CN 8 seems to be an unlikely candidate as well, as none of the participants noted any subjective sense of vertigo or dysequilibrium with insufflation, and there appeared to be no objective signs, i.e. nystagmus, which would indicate unilateral vestibular activation or de-activation.

This proposition leads to our second question which pertains to the innervation of the non-labyrinthine structures involved and their central afferent projections. It is known that innervation of this anatomy is carried via multiple structures and that the tympanic membrane itself is highly sensitive to changes in external pressure (Figure 3). The auriculotemporal nerve, via the mandibular nerve of CN 5 supplies not only the anterior half of the membrane, but is also the chief somatosensory afferent fiber of the tympanic membrane. The posterior portion of the tympanic membrane is innervated by the auricular branch of CN 10. The tympanic branch of CN 9 also innervates these structures, but to a lesser degree [41,42].

There are potentially significant implications in this neuroanatomical understanding [43]. Knowing that migraines are propagated and maintained in part, through dysfunction of the trigeminocervical system, it seems as though we are observing a way to directly access and modulate that system by way of trigeminal afferents from the tympanic membrane. This particular pathway might have a particular affinity for influencing aberrant patterns of brainstem activity and integration. This scenario seems to be the most likely based upon our current understanding of the neuroanatomy of the trigeminal system, its pathopysiological contribution to migraine and its afferent and efferent projections [44-47].

The third question arises from the previous and involves exactly which central ascending and descending pathways are activated during this particular stimulation and what other cortical areas are involved (Figure 4). We can presume, through fundamental neuroanatomy, that the auriculotemporal nerve reaches the chief sensory nucleus of the trigeminal nerve in the pontine reticular formation and initially exerts effects on local neuronal pools.

Ascertaining which cortical networks become activated secondarily, in relation to pain modulation and other migraine symptoms, would certainly be of great value in understanding the mechanisms underlying the efficacy of this procedure. What needs to be elucidated next are the pertinent neurochemical mediators, anatomical relationships and suprasegmental modulatory networks which can fully explain the observations described here [48-55].


Figure 3. Distribution of the maxillary and mandibular nerves, and the submaxillary ganglion.

Figure 4. Mandibular division of the trigeminal nerve.


Multiple studies have demonstrated the effectiveness of various modes of stimuli on the amelioration of some neurological conditions [11,22 -25,27-30,32,36]. Adding more credence to these observations are investigations utilizing functional magnetic resonance imaging techniques which have demonstrated distinct patterns of cortical activation associated with those applications and stimulations [16-21]. It seems very clear now that there is a real and significant relationship between brainstem activation and cortical areas known to be affected by, and modulate the experience of pain and suffering.

The final issue, which naturally arises in examining the current data, is the breadth of symptomatic change and the immediacy the results obtained with one simple application. This would certainly suggest a role of the central nervous system, rather than strictly vascular dynamics, in the propagation and resolution of migraines headaches. Certainly, pneumatic insufflation to the external ear does not introduce exogenous vasoactive mediators to the system, but rather might provoke beneficial changes including activation of brainstem nuclei and optimized cortical metabolism which then lead to more adaptive function of associated intra-cranial structures and ultimately, normalized function. If this ‘direct control’ method through pontomedullary centers can be substantiated, it would tend to de-emphasize the understanding of migraines as an event sustained largely by nociceptive activation of fibers surrounding intra-cranial vascular tissue. What remains then, is to thoroughly elucidate the mechanisms by which this application exerts its effects and how it relates to the current understanding of migraine pathophysiology.

CONCLUSION

The clinical data and observations produced by the current study support, very compellingly, that pressure induced trigeminal activation via pneumatic ear insufflation can significantly alter the pain and concomitant symptoms associated with migraine headaches. To our knowledge, this is the first time within the full body of the neurological literature that the therapeutic application of pneumatic ear insufflation has been shown to be effective in rapidly reducing or resolving the pain and concomitant features of migraine headache.

The results of the current study are certainly enticing to the possibility that such a simple, non-invasive, inexpensive and easily repeatable procedure could afford such rapid and dramatic reduction in migraine pain levels. It raises the question: What if pneumatic ear insufflation could be beneficial for not just palliative relief, but as a therapy which could produce long-term resolution of migraines if repeated with some degree of frequency? Furthermore, it is a logical and exciting thought to wonder what other types of pain and neurological dysfunction can be ameliorated or resolved with this form of stimulation [56,57]. Other states of central pain and dysfunction share overlapping symptomatology with migraine headaches and could potentially benefit from this type of stimulation as well.

The efficacy of this procedure will certainly need to be validated and demonstrated with repetition on many more subjects. Future investigations would be well advised to explore this type of therapy in blinded, controlled type of evaluation. Certainly, this application might not benefit every instance and type of migraine headache, but continued research might help determine the criteria and selection of patients who might be good or poor candidates for this type of intervention.

Finally, the results obtained in this investigation offer further credibility and support for the growing body of data regarding the ‘functional’ approach to neurorehabilitation [12]. The driving force within this field is the dynamic changeability of the function of the human nervous system and how to alter it when maladaptive changes impact an individual’s quality of life. Because it is well known that the function of the nervous system can be altered through chemical, electrical, structural, genetic, immunological, hormonal and other factors [12], knowledge of all of these aspects can profoundly aid clinicians and researchers in mankind’s progress to understanding and developing new and more effective interventions for chronic neurological diseases. It is the hope of the author that this movement will continue to progress in its scope and reach, in order to deliver more useful and effective interventions for disease of the human condition.

 

REFERENCES

  • Buse D, Manack A, Serrano D, Reed M, Varon S, Turkel C, Lipton R. Headache impact of chronic migraine and episodic migraine: results from the American Migraine Prevalence and Prevention Study. Headache: J Head Face Pain. 2012;52:3-17.
  • Diener HC, Dodick DW, Goadsby PJ, Lipton RB, Olesen J, Silberstein SD. Chronic migraine-classification, characteristics and treatment. Nat Rev Neurol. 2012;8(3):162-71.
  • Breslau N, Schultz L, Lipton R, Peterson E, Welch KMA. Migraine headaches and suicide attempt. Headache: J Head Face Pain. 2012;52(5):723-731.
  • Peroutka S.The Pharmacology of Current Anti-Migraine Drugs. Headache: The Journal of Head and Face Pain. 1990;30:5–11.
  • Bozoghlanian M, Vasudevan SV. Overview of migraine treatment. Pain Management. 2012;2(4):399-414.
  • Goldberg LD. The cost of migraine and its treatment. Am J Manag Care. 2005;11:S62-S67.
  • Magis D, Schoenen J. Advances and challenges in neurostimulation for headaches. Lancet 2012;8(3):162-71.
  • Ashkenazi A, Levin M. Greater occipital nerve block for migraine and other headaches: is it useful? Curr Pain Headache Rep. 2007;11(13):231-5.
  • Caputi CA, Firetto V. Therapeutic blockade of greater occipital and supraorbital nerves in migraine patients. 1997;37(3):174-9.
  • Robertson CE, Garza I. Critical analysis of the use of onabotulinumtoxin A (boluilinum toxin type A) in migraine. Neuropsychiatr Dis Treat. 2012;8:35-48.
  • Perini F, De Boni A. Peripheral neuromodulation in chronic migraine. Neurolog Sci. 2012;33(Supp1):29-31.
  • Leisman G. Brain networks, plasticity, and functional connectivities inform current directions in functional neurology and rehabilitation. Func Neurol Rehab Ergon. 2011;1(2):315-356.
  • Beck RW. Functional neurology for practitioners of manual therapy. Elsevier Health Sciences; 2008:8. 
  • Carrick FR. Changes in brain function after manipulation of the cervical spine. J Manipulative Physiol Ther. 1997;20(8):529-45.
  • Beck RW. Functional neurology for practitioners of manual therapy. Elsevier Health Sciences;2008:156.
  • Suzuki M, Kitano H, Ito R, Kitanishi T, Yazawa Y, Ogawa T, Shiino A, Kitajima K. Cortical and subcortical vestibular response to caloric stimulation detected by functional magnetic resonance imaging. Brain Res Cogn Brain Res. 2001;12(3):441-9.
  • Bucher SF, Dieterich M, Wiesmann M, Weiss A, Zink R, Yousry T, Brandt T. Cerebral functional magnetic resonance imaging of vestibular, auditory, and nociceptive areas during galvanic stimulation. Ann Neurol. 1998;44(1):120-5.
  • Miyamoto T, Fukushima K, Takada T, de Waele C, Vidal PP. Saccular projections in the human cerebral cortex. Ann NY Acad Sci. 2005;1039:124-31.
  • de Waele C, Baudonniere PM, Lepecq JC, Tran Ba Huy P, Vidal PP. Vestibular projections in the human cortex. Exp Brain Res. 2001;141(4):541-51.
  • Klingner CM, Volk GF, Flatz C, Brodoehl S, Dieterich M, Witte O, Guntinas-Lichius O. Components of vestibular cortical function. Behav Brain Res. 2013;236:194-199.
  • Fasold O, von Brevern M, Kuhberg M, Ploner CJ, Villringer A, Lempert T, Wenzel R. Human vestibular cortex as identified with caloric stimulation in functional magnetic resonance imaging. 2002;17(3):1384-93.
  • Rode G, Vallar G, Revol P, Tilikete C, Jacquin-Courtois S, Rossetti Y, Farnè A. Facial macrosomatognosia and pain in a case of Wallenberg’s syndrome: selective effects of vestibular and transcutaneous stimulations. 2012;50(2):245-53.
  • Ramachandran, VS, McGeoch PD, Williams L, Arcilla G. Rapid relief of thalamic pain syndrome induced by vestibular caloric stimulation. Neurocase. 2007;13(3):185-8.
  • McGeoch PD, Williams LE, Lee RR, Huang M, Ramachandran VS. Post-stroke tactile allodynia and its modulation by vestibular stimulation: a MEG case study. Acta Neurol Scand. 2009;119(6):404-9.
  • McGeoch PD, Ramachandran VS. Vestibular stimulation can relieve central pain of spinal origin. Spinal Cord. 2008;46(11):756-7.
  • LeChapelain L, Beis JM, Paysant J, Andre JM. Vestibular caloric stimulation evokes phantom limb illusions in patients with paraplegia. Spinal Cord. 2001;39(2):85-87.
  • Kolev O. How caloric vestibular irritation influences migraine attacks. 1990;10(4):167-9.
  • Baguley DM, Knight R, Bradshaw L. Does caloric vestibular stimulation modulate tinnitus? Neurosci Lett. 2011;492(1):52-4.
  • Furman, JM, Sparto PJ, Soso M, Marcus D. Vestibular function in migraine-related dizziness: a pilot study. J Vest Res. 2005;15(5-6):327-32.
  • Holm AF, Staal MJ, Mooij JJ, Albers FW. Neurostimulation as a new treatment for severe tinnitus: a pilot study. Otol Neurotol. 2005;26(3):425-8.
  • Londero A, Chays A. Tinnitus treatment: neurosurgical management. 2009;55(2):248-58.
  • Bartels H, Staal MJ, Holm AF, Mooij JJ, Albers FW. Long-term evaluation of treatment of chronic, therapeutically refractory tinnitus by neurostimulation. Stereotact Funct Neurosurg. 2007;85(4):150-7.
  • Andre JM, Martinet N, Paysant J, Beis JM, LeChapelain L. Temporary phantom limbs evoked by vestibular caloric stimulation in amputees. Neuropsychiatry Neuropsychol Behav Neurol. 2001;14(3):190-6.
  • Seemungal B, Rudge P, Davies R, Gretsy M, Bronstein A. Three patients with migraine following caloric-induced vestibular stimulation. J Neurol. 2006;253(8):1000-1.
  • Baier B, Stieber N, Dieterich M. Vestibular evoked myogenic potentials in vestibular migraine. J Neurol. 2009;256(9):1447-54.
  • Bottini G, Paulesu E, Gandola M, Loffredo S, Scarpa P, Sterzi R, Santilli I, Defanti CA, Scialfa G, Fazio F, Vallar G. Left caloric vestibular stimulation ameliorates right hemianesthesia. 2005;65(8):1278-83.
  • Goadsby PJ, Lipton RB, Ferrari MD. Migraine. Current Understanding and Treatment. N Engl J Med 2002;346:257-270.
  • Bolay H. Reuter U, Dunn AK, Huang Z, Boas DA, Moskowitz MA. Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nat Med. 2002;8(2):136-142.
  • Goadsby PJ, Zagami AS, Lambert GA. Neural processing of craniovascular pain: a synthesis of the central structures involved in migraine. 1991;31(6):365-371.
  • Kandel E, Schwartz J, Jessell T. Principles of neural science. 4th ed. New York: McGraw Hill;2000:595.
  • Dirckx JJ, Decreamer WF. Human tympanic membrane deformation under static pressure. Hear 1991;51(1):93-105. 
  • Lim DJ. Structure and function of the tympanic membrane: a review. Acta Otorhinolaryngol 1995;49(2):101-15.
  • Komarrnitki I, Andrzejczak-Sobocińska A, Tomczyk J, Deszczyńska K, Ciszek B. Clinical anatomy of the auriculotemporal nerve in the area of the infratemporal fossa. Folia Morphol. 2012;71(3):187-93.
  • Porta-Etessam J, Garcia-Cobos R, Cuadrado ML, Cassanova I, Lapeña T, Garcia-Ramos R. Neuro-otological symptoms in patient with migraine. Neurologia. 2011;26(2):100-4.
  • Burstein R, Cutrer MF, Yarnitsky D. The development of cutaneous allodynia during a migraine attack: clinical evidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine. Brain. 2000;123(Pt 8):1703-9.
  • Chim H, Okada C, Brown MS, Alleyne B, Liu M, Zwiebel S, Guyuron B. The auriculartemporal nerve in etiology of migraine headaches: compression points and anatomical variations. Plast Recon Surg. 2012;130(2):336-41 
  • Janis JE, Hatef DA, Ducic I, Ahmad J, Wong C, Hoxworth R, Osborn T. Anatomy of the auriculotemporal nerve: variations in its relationship to the superficial temporal artery and implications for the treatment of migraine headaches. Plast Recon Surg. 2010;125950:1422-28. 
  • Broman J. Neurotransmitters in subcortical somatosensory pathways. Anat Embryol. 1994;189:181-214.
  • Moskowitz MA, Romero J, Reinhard JF, Melamed E, Pettibone DJ. Neurotransmitters and the fifth cranial nerve: is there a relation to the headache phase of migraine? 1979;314(8148):883-5.
  • Oshinsky ML, Luo J. Neurochemistry of trigeminal activation in an animal model of migraine. 2006;46(Supp1):S39-44.
  • Lazarov NE. Comparative analysis of the chemical neuroanatomy of the mammalian trigeminal ganglion and mesencephalic trigeminal nucleus. Prog Neurobiol. 2002;66(1):19-59.
  • Bae YC, Ihn HJ, Park MJ, Ottersen OP, Moritani M, Yoshida A, Shigenaga Y. Identification of signal substances in synapses made between primary afferents and their associated axon terminals in the rat trigeminal sensory nuclei. J Comp Neurol. 2000;418(3):299-309.
  • Hayar A, Poulter MO, Pelkey K, Feltz P, Marshall KC. Mesencephalic trigeminal neuron responses to gamma-aminobutyric acid. Brain Res. 1997;753(1):120-7.
  • D’Andrea G, Leon A. Pathogenesis of migraine: from neurotransmitter to neuromodulators and beyond. Neurol Sci. 2012;31(Supp 1):S1-7.
  • Dal Bo G, Lund JP, Verdier D, Kolta A. Inputs to nucleus caudalis from adjacent trigeminal areas. Eur J Neurosci. 2005;22(8):1987-96.
  • Stuginski-Barbosa J, Murayama RA, Conti PCR, Speciali JG. Refractory facial pain attributed to auriculotemporal neuralgia. J Headache Pain. 2012;13(5):415-17.
  • Bayazit YA, Gursoy S, Ozer E, Karakurum G, Madenci E. Neurotologic manifestations of the fibromyalgia syndrome. J Neurol Sci. 2002;196(1-2):77-80.

 

 

Received: January 2 2013 Revised: January 28 2013 Accepted: February 15 2013.