Month: May, 2018

Simply exactly what are Headaches

May 31, 2018 Uncategorized 1 Comment

Precisely exactly what are Headaches

Statistics specify that aggravation is amongst among one of the most common conditions experienced by people not simply in the United States yet in addition of those that are staying in numerous elements of the world. Research study research studies furthermore expose that a significant percent of people from numerous areas are in addition big consumers of different painkiller– the initial aid in reducing migraine headache.

Professionals declare that there are different sort of migraine headache that are mapped to numerous factors. If you are just one of those that experiences irritations often, perhaps it’s presently time to lengthen your knowledge worrying the regular illness along with discover specifically just what you might do to completely get rid of migraine headache in your life.


As defined, disappointment explains the pain in any type of kind of element of a person’s head. Migraine headaches are experienced when exhaustion along with stress, muscular tissue anxiety, increased capillary, along with others advertise the delicate nerve fibers uncovered in the head.

Experts consent that migraine headaches can be recognized to migraine frustration aggravations which explain the type of persisting in addition to severe migraine headache that has severe vibrating on the sanctuaries, a sick stomach along with harmed vision; collection irritations which are specified to birth similarities to migraine frustrations simply they are knowledgeable put simply durations in addition to take place daily over weeks or months; and anxiety aggravations that explains the sort of migraine headache that might strike continuous location in addition to bring about tightenings up of the face, scalp, or neck muscular tissue mass.

Aggravations are also determined as vascular, tightening or stress and anxiety, grasp and inflammatory. Specialists assert that vascular aggravation explains the involved unusual function of the person’s vascular system or mind’s vein while tightening migraine headache consist of the company or having of the muscles in the person’s face and neck.

Hold along with inflammatory stress, on the numerous other hand, are considered as symptoms and signs of different other connected problems such as infection, stroke as well as numerous other significant neurological problems.

Experts assert that the treatment of disappointment depends primarily on its factor. Among one of the most regular aggravation treatment out there is taking control of the counter drugs such as anesthetics like pain medication as well as acetaminophen. Others suggest normal migraine headache therapies like making use of cozy or trendy compresses, exercise, adequate remainder, appropriate die, and regular exercise to avoid regular migraine headaches.

If your migraine headache still does not disappear after doing these simple treatments, ask your healthcare business or doctor to assess you thoroughly so right medication is offered in circumstance your migraine headache is a result of an additional complicated issue.

Specialists specify that there are different sort of stress that are mapped to different factors. If you are just one of those that experiences irritations regularly, perhaps it’s presently time to increase your competence concerning the common illness along with reveal simply exactly what you can do to definitely remove irritation in your life.

Others advise common migraine headache therapies like utilizing cozy or cool compresses, exercise, ample remainder, suitable die, as well as typical exercise to remain free from constant migraine headaches.

Recovering Headaches

May 31, 2018 Uncategorized 1 Comment

Recovering Headaches

Consistent migraine headache attacks can develop one to lose out on crucial days from establishment or work as well as could similarly impede individuals from spending valuable time with taken pleasure in ones along with can additionally restrain social dedications. It is incredibly crucial to get the ideal clinical diagnosis for the factor of the migraine headaches in addition to acquire the proper treatment as well as migraine treatment.

In circumstances like these, it is incredibly convenient to get the technique of bearing in mind of one’s migraine headache with using a stress journal. The worth of appropriately spotting the resource of the migraine headache can not be fretted adequate because of that it is not simply important to get the very best treatment in addition to therapy yet typically, disappointments are indicators of a whole lot a lot more substantial ailment.

Migraine headaches are really normal as well as millions after numerous individuals around the world truly withstand from relentless to routine migraine headaches, there is no variable to take this carefully. There a number of significant migraine headache produces offered that are really normal, like collection irritations, sinus migraine headaches and migraine frustration. While all these are benign or are migraine headaches that are not fatal, the relentless attacks from these create episodes of run-down lives in addition to this not call for apply.

There are a selection of exceptionally reliable migraine headache therapies readily available for additionally among one of the most likewise consistent as well as severe aggravation. Typically, the factor that stress solutions do not feature is that an individual may be taking imprecise medication.

Research study research studies have really validated that a lot of individuals whine that sinus migraine headache treatments do not operate on them and this is simply considering that numerous people that presume they experience from sinus migraine headaches are actually sustaining from migraine frustration. This is why the aggravation therapy they are taking do not work.

Keeping in mind and logging details concerning your irritation attacks can help you connect and remember your disappointments better for proper physician clinical diagnosis. Simply just what’s much more is that a stress journal is an exceptional approach for you to be able to uncover patterns that you can not have really seen in the past.

Preserving a migraine headache journal might help the exclusive become a lot more aware of factors that are happening that they might not keep in mind of otherwise for the aggravation journal. Because of that this will absolutely aid you as well as your doctor appropriately discover simply exactly what the difficulty absolutely is, keeping a migraine headache journal hassle-free is the preliminary activity to the very crucial disappointment therapy and treatment.

It is actually necessary to get the appropriate clinical diagnosis for the factor of the migraine headaches in addition to acquire the ideal treatment in addition to stress therapy.

Migraine headaches are extremely normal in addition to millions after numerous individuals worldwide actually experience from relentless to regular irritations, there is no element to take this delicately. There a few major migraine headache develops available that are instead normal, like collection stress, sinus irritations in addition to migraine frustration.

Problem of Being a Lady in addition to Having Frustrations along with hormone representatives

May 31, 2018 Uncategorized 1 Comment

Dilemma of Being a Woman as well as Having Headaches and hormone representatives

It is an unidentified (or little recognized) reality that girls experience are more than likely to experience migraine headaches as compared to men do.

Scientific research study assumes that women may have added painful irritations compared with people. Typically, there are a range of components that

gone into play when thinking of an individual’s chances of developing aggravations, along with the consistency of such concerns. Age,

genetics, and relative history might all add, nonetheless, for women, there are a couple of numerous other variables to be thought of.

Hormone representative levels along with birth control pill (which damages existing levels or existing fabricated hormone representatives to the body) are

both possible think about the migraine headache formula.

As defined, there many variables that can add in someone’s chances of acquiring disappointments. Age appears

to be a big facet. The older one obtains, theoretically, the a lot more at risk one is to experiencing aggravations. People with a member of the family

history of going to threat to the concern are also at elevated threat, though whether there is a concrete genetic

internet link is still unforeseeable. Ladies have in fact involved remember that modifications in hormone representatives can generally be included by migraine headaches.

This might contain factors like certain periods of the menstrual cycle, pregnancy, and various other times or problems that

change a woman’s usual hormone representative levels. This contains the use (or overuse) of birth control pill in addition to places, which offer

synthetic hormone representatives.

The very easy origin of this would absolutely be progesterone in addition to estrogen, sometimes described as the core hormone representatives of the females physiology.

Both of them could have an effect on numerous other chemicals in the body, along with a variety of chemical receptors. Among the a number of

viable physical materials that can be influenced by the 2 mentioned above are the ones that collaborate with along with control

migraine headaches psychological. This typically happens as an outcome of some kind of “interaction” with numerous other chemicals psychological. For

circumstances, high levels of estrogen in addition to decreased levels of serotonin have really been identified to develop aggravations in some individuals, with the

toughness varying from the light to the extreme. As might be expected, there are times when the fabricated hormone representatives of birth

control tablet computers can in addition have similar outcomes.

Also if hormone representative levels are a natural element of the body as well as likewise could not be tossed out completely does not suggest the

regular woman is vulnerable versus them. Modern drug has indicates handy manage– or quit, possibly– the

migraine headaches. A great deal of non-prescription medicine all set approaches of combating migraine headaches that come throughout the start of

menstruation, which is usually accompanied by a sudden reduction in estrogen levels. Proper diet plan routine as well as exercise, which are

basically taken into account to be terrific for virtually anything, might furthermore assist in lowering the toughness of hormone-related aggravations

when they come. Appropriate in addition to proper remainder can in addition be critical in this.

Precisely just what worrying those that take advantage of birth control pill? There are approaches to get rid of off hormone-related stress for women on the tablet computer,

The suggestions can be a little numerous from those of ladies that generally aren’t. Taking a program that has basically sugar tablet

days might be helpful in helping battle the feasible increase in hormonal agent migraine headaches. There are furthermore tablet computers and identifies that do

not use estrogen or progesterone, in addition to for this reason there is no improved hazard of aggravations.

The older one obtains, theoretically, the much more vulnerable one is to experiencing migraine headaches. People with a home

This usually takes place as a result of some kind of “record” with different other chemicals psychological.

The older one obtains, in concept, the also extra susceptible one is to experiencing irritations. People with a household participants

This generally takes location as an outcome of some kind of “interaction” with different other chemicals in the mind.

PMS and also migraine headaches

May 31, 2018 Uncategorized 0 Comments

PMS as well as migraine headaches

No person understands specifically just what triggers migraine headache frustrations, and even exactly what takes place in the body as well as mind when somebody has one. One point that is recognized, nevertheless, is that 3 times as several ladies as males have migraine headaches. Several women migraineurs will certainly likewise admit that their frustrations are most likely to accompany the duration right before their menstruation duration.

A massive sixty percent of females migraineurs have migraine headaches throughout their duration and also throughout the remainder of the month. Fourteen percent just have a migraine frustration throughout their duration. Consider the numbers; seventy-four percent of all ladies migraineurs connect their duration with their migraines, and also while clinical scientific research does not refute the link, the factor for it is still unidentified.

On top of that, several females that come to be migraineurs later on in life state that their pre-menstrual disorder (PMS) signs ended up being far more intense because the frustrations started. A research released in the January 2006 problem of Headache validated the apocryphal proof. Females getting involved reported that bloating, weight gain, bust inflammation, state of mind swings, neck and back pain, as well as stomach aches all came to be extra serious throughout a migraine headache.

The females in the research were offered a medicine to generate a short-term man-made menopause by stopping the activity of the ovaries. Despite the hormone ups and also downs of routine durations gotten rid of, they still reported intensified PMS signs throughout a migraine headache assault.

The fourteen percent of females that just have migraine headaches throughout their duration are claimed to have “menstruation migraine headaches”. For some fortunate ladies, taking a quick program of NSAIDs (non-steroidal anti-inflammatory medications, like advil) for a number of days prior to their duration as well as the initial couple of days of it could stave off a menstruation migraine headache.

A monstrous sixty percent of females migraineurs have migraine headaches throughout their duration as well as throughout the remainder of the month. The fourteen percent of females that just have migraine headaches throughout their duration are claimed to have “menstruation migraine headaches”. For some fortunate females, taking a quick training course of NSAIDs (non-steroidal anti-inflammatory medications, like advil) for numerous days prior to their duration as well as the very first couple of days of it could stave off a menstruation migraine headache.

I have a migraine headache disappointment

May 31, 2018 Uncategorized 1 Comment

I have a migraine headache disappointment

I’ve been around various people that make use of words Migraine, when they talk relating to having a headeache. Do these people as a matter of fact have migraine headache frustrations?

Words “migraine frustration” stems from the Greek word “hemikranion” which relates to “pain affectin one side of the head”. A Migraine is a stress in a kind, that is generally truly strong along with might almost be disabling, when extreme. Unlike commong stress’s which everyone is at risk to, migraine frustrations are a neurologic problem, in addition to among one of the most normal type of vascular disappointment.

Everyone details influenced by migraine headache frustrations will absolutely recognize the check in a various method, the magazine states: severe pain on one or perhaps a lot more sides of the head, a troubled stomach, and sometimes interfered with vision. The difference between a disappointment and migraine frustration is summed up in words “Aura”, which explains the migraine frustration showcases that are non-headache like. Migraine frustrations have really existed throughout history, as well as it is acknowledged that relative history in addition to genetic facets are essential in the likelyhood of migraine headache frustrations.

Many doctors take care of migraine headache frustrations, in addition to will definitely have many a good idea treatment for migraine headache frustrations. It remains in my experience that nonprescription pain awesomes, along with numerous other medicines have their part in reducing the pain migraine headache frustrations produce, yet are never ever before actually able to recover them. Speak to your doctor, along with others that have in fact knowledgeable migraine headache frustrations, to uncover out specifically just what activities might be best for you.

Unlike commong migraine headache’s which everyone is at risk to, migraine frustrations are a neurologic problem, in addition to one of the most normal sort of vascular stress.

The difference between a migraine headache in addition to migraine frustration is summarized in words “Aura”, which describes the migraine frustration showcases that are non-headache like. Migraine frustrations have really been existing throughout history, along with it is identified that family history as well as genetic facets are essential in the likelyhood of migraine headache frustrations.

A number of physician manage migraine headache frustrations, along with will absolutely have countless recommended treatment for migraine headache frustrations.

The difference in between an aggravation as well as likewise migraine frustration is summed up in words “Aura”, which defines the migraine frustration showcases that are non-headache like. Migraine frustrations have really existed throughout history, as well as likewise it is acknowledged that household participants history as well as genetic facets are really crucial in the likelyhood of migraine headache frustrations.

Many medical professionals deal with migraine headache frustrations, as well as will definitely have various recommended treatment for migraine headache frustrations.

The Four Phases of Migraines

May 30, 2018 Uncategorized 1 Comment

The Four Phases of Migraines

Migraines are a neurological disease, of which the most common symptom is an intense and disabling episodic headache. Migraines are usually characterized by severe pain on one or both sides of the head and are often accompanied by hypersensitivity to light, hypersensitivity to sound and nausea.

The signs and symptoms of migraine vary among persons. Therefore, what a person experiences before, during and after an attack cannot be defined exactly. The four “signs and symptoms” below are common among persons but are not necessarily experienced by all migraine sufferers:

1.The prodrome, which occurs hours or days before the headache.

2.The aura, which immediately precedes the headache.

3.The headache phase.

4.The postdrome.

The first phase or prodrome

Prodromal symptoms occur in 40% to 60% of migraineures. This phase consists of altered mood, irritability, depression or euphoria, fatigue, yawning, excessive sleepiness, craving for certain food (e.g., chocolate), and other vegetative symptoms. These symptoms usually precede the headache phase of the migraine attack by several hours or days and experience teaches the person or observant family that the migraine attack is near.

The second phase or the Aura

The migraine aura is comprised of focal neurological phenomena that precedes or accompany the attack. They appear gradually over 5 to 20 minutes and usually subside just before the headache begins. Symptoms of migraine aura are usually sensory in nature.

Visual aura is the most common of the neurological events. There is a disturbance of vision consisting usually of unformed flashes of white or rarely of multicolored lights (photopsia) or forma­tions of dazzling zigzag lines (arranged like the battlements of a castle, hence the term fortification spec­tra or teichopsia).

Some persons complain of blurred or shimmering or cloudy vision, as though they were look­ing through thick or smoked glass. The somatosensory aura of migraines consist of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm as well as in the ipsilateral nose-mouth area. Paresthesia migrate up the arm and then extend to involve the face, lips and tongue.

The third phase: The Headache

The typical migraine headache is unilateral, throbbing, moderate to severe and can be aggravated by physical activity . Not all of these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, usually alternates sides from one attack to the next.

The onset is usually gradual. The pain peaks and then subsides, and usually lasts between 4 and 72 hours in adults and 1 to 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several times a week, and the average migraineur experiences from one to three migraines a month.

The head pain varies greatly in intensity. The pain of migraines is invariably accompanied by other features. Anorexia is common, and nausea occurs in almost 90 percent of persons, while vomiting occurs in about one third of persons.

Many persons experience sensory hyperexcitability manifested by photophobia, phonophobia, osmophobia and seek a dark and quiet room. Blurred vision, nasal stuffiness, diarrhea, polyuria, pallor or sweating may be noted during the headache phase. There may be localized edema of the scalp or face, scalp tenderness, prominence of a vein or artery in the temple, or stiffness and tenderness of the neck. Impairment of concentration and mood are common. Lightheadedness, rather than true vertigo and a feeling of faintness may occur. The extremities tend to be cold and moist.

The fourth phase: postdrome phase

The person may feel tired, “washed out”, irritable, listless and may have impaired concentration, scalp tenderness or mood changes. Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise.

The information presented here should not be interpreted as medical advice. If you or someone you know suffers from migraines, please seek professional medical advice for the latest treatment options.

Permission is granted to reprint this article as long as no changes are made, and the entire resource box is included.

Transformed Migraine

May 28, 2018 Uncategorized 1 Comment

Transformed Migraine

Migraine headaches bring some of the most excruciating pain a person will ever know. Many migraineurs say the only good thing about a migraine is the relief, sometimes even euphoria, they feel when the headache is over. Knowing that a good feeling is waiting on the other side is the only thing that helps some of them get through the pain.

People who live with transformed migraine (TM) do not have anything to look forward to. Transformed migraine is the name of a condition some migraineurs develop after years of migraine episodes. Most people develop transformed migraines in their 20s or 30s.

Migraineurs report less severe headaches suddenly, but they come more often until they turn into chronic daily headaches (CDH). The daily headache is less intense than a migraine episode, but still painful, and most transformed migraine patients still have occasional full-blown migraine episodes.

Not all migraineurs will develop transformed migraines. In fact, most won’t. Those who do are predominantly women and approximately 90% of them previously had migraine with aura (classic migraine). Migraine with aura is relatively rare, affecting less than 20% of all migraineurs.

The exact cause of transformed migraines is, like all migraine types, unknown. Many transformed migraineurs are heavy users of pain-relievers, both over the counter items like acetaminophen and naproxen and prescription medications like Vicodin or Darvon. Some even take them daily, whether they have a migraine or not, thinking they may help prophylactically.

TM patients of this type are particularly hard to treat because of a developed tolerance for pain medication. The first step in treating these patients is to wean them from their daily medications. Sometimes this step alone will stop the chronic lesser headaches. Once weaned, like non-medication dependent TM patients, their migraines are manageable with a regular treatment regimen just like any other migraineur.

Research Submission

May 23, 2018 alex News Tags: 1 Comment

[googlepdf url=”” ]

ISSN 0017-8748
doi: 10.1111/head.13318
V 2018 American Headache Society
Published by Wiley Periodicals, Inc.

Research Submission



Resting State Functional Connectivity After Sphenopalatine Ganglion Blocks in Chronic Migraine With Medication Overuse Headache: A Pilot Longitudinal fMRI Study


Kaitlin Krebs, MSc; Chris Rorden, PhD; X. Michelle Androulakis, MD, MSc



Objective.—In this pilot study, the purpose is to investigate if a series of sphenopalatine ganglion (SPG) blockade treatments modulate the functional connectivity within the salience and central executive network (CEN) in chronic migraine with medication overuse headaches (CMw/MOH).


Background.—Using intranasal local anesthesia to block the SPG for the treatment of various headache disorders has been employed in clinical practice since the early 1900s. However, the exact mechanism of how SPG modulate resting state intrinsic functional brain networks connectivity remains to be elucidated. This pilot study seeks to understand the resting state connectivity changes in salience and CENs, with emphasis on the mesocorticolimbic systems, before and after a series of SPG block treatments.


Methods.—Using fMRI, resting state connectivity was derived from predefined networks of nodes (regions of inter-ests) for the salience (27 nodes, 351 connections) and CENs (17 nodes, 136 connections). After treatments, a paired sam-ples t-test (with 10,000 permutations to correct for multiple comparison) was used to evaluate changes in the intranetwork resting state functional connectivity within the salience and executive networks, as well as the overall network connectivity strength.


Results.—When comparing connectivity strength at baseline to that at the end of treatment in our cohort of 10 CMw/ MOH participants, there were several connections within the salience (n 5 9) and executive (n 58) networks that were sig-nificantly improved. Within the salience network, improved connectivity was observed between the prefrontal cortex and various regions of the insula, basal ganglia, motor, and frontal cortex. Additionally, changes in connectivity were observed between regions of the temporal cortex with the basal ganglia and supramarginal gyrus. Within the CEN, improved connec-tivity was observed between the prefrontal cortex and regions of the anterior thalamus, caudate, and frontal cortex. After treatment, the overall CEN connectivity was significantly improved (Baseline 0.00 60.08; 6 weeks 0.03 6 0.09, P 5.01); however, the overall salience network connectivity was not significantly improved (Baseline 20.01 60.10; 6 weeks


0.01 60.12, P 5.26). Additionally, after treatment, there was a significant reduction in the number of moderate/severe


headache days per month (Baseline 21.1 66.6; 6 weeks 11.2 6 6.5, P < .001), HIT-6 (Baseline 66.1 62.6; 6 weeks 60.2 63.6, P < .001), and PHQ-9 (Baseline 12.4 65.7; 6 weeks 6.1 63.6, P 5 .008) scores.


Conclusion.—In this longitudinal fMRI study, we observed improved functional connectivity within both networks, pri-marily involving connectivity between regions of the prefrontal cortex and limbic (cortical-limbic) structures, and between different cortical (cortical-cortical) regions after a series of repetitive SPG blockades. The overall CEN strength was also





From the School of Medicine, Department of Neurology, University of South Carolina, Columbia, SC, USA.


Address all correspondence to X.M. Androulakis, University of South Carolina School of Medicine, Department of Neurology, Columbia, SC 29203.


Accepted for publication March 11, 2018.



improved. Our results suggest that recurrent parasympathetic inhibition via SPG is associated with improved functional connectivity in brain regions critical to pain processing in CMw/MOH.


Key words: salience network, central executive network, fMRI, chronic migraine, sphenopalatine ganglion, resting state connectivity


Abbreviations:   ASC 12 allodynia symptom checklist, aPFC anterior PFC, BOLD blood oxygenation level dependent, CEN central executive network, CM chronic migraine, CMw/MOH chronic migraine with medication over-use headaches, dACC dorsal anterior cingulate cortex, dCaudate dorsal caudate, dmPFC dorsal medial PFC, dPFC/FEF dorsal PFC/frontal eye field, dlPFC dorsolateral prefrontal cortex, TE echo time, EA extended amygdala, FOV field of view, HIT-6 headache impact test, IFG inferior frontal gyrus, MP-RAGE magnetization-prepared rapid gradient echo, MNI Montreal Neurological Institute, NTNC node to node connectivity, NSAIDs nonsteroidal anti-inflammatory drugs, OFI orbitofrontal insula, PHQ-9 Patient Health Questionnaire, PAG periaqueductal gray, PFC prefrontal cortex, ROIs region of interest, TR repe-tition time, SN salience network, SPG sphenopalatine ganglion, SSN superior salivatory nucleus, SMA sup-plementary motor area, SMG supramarginal gyrus, vSP ventral striatum/pallidum, VTA/SNPC ventral tegmental area/Substantia nigra, vlPFC ventrolateral PFC, vmCaudate ventromedial caudate


(Headache 2018;58:732-743)




Sphenopalatine ganglion (SPG) plays a crucial role in migraine pathogenesis through activation of the trigemino-autonomic reflex.1,2 Parasympathetic nerves arise from superior salivatory nucleus (SSN) synapses on the SPG, where postsynaptic afferents from the SPG then trigger vasodilatation of the cra-nial and meningeal vasculature, subsequently leading to a cascade of neuroinflammatory events that initiate migraine pain and associated autonomic symptoms.3 Via its connection with the SSN, SPG has indirect link with the limbic systems and cortical regions, which are often affected in migraine populations.3-5 Intranasal application of local anesthesia to the SPG is efficacious for acute pain relief, improving migraine related disability at 6 weeks post treatment.6,7 The exact mechanism of SPG neuromodulation remains to be elucidated. Decreased parasympathetic outflow from the SPG block, especially in the frontal regions of the brain, is likely crucial for improved migraine pain and related symptoms.8


Our lab conducted a recent study that revealed decreased overall functional connectivity in default


Conflict of Interest: Kaitlin Krebs and Chris Rorden do not report any conflicts of Interest. Michelle Androulakis disclo-ses that she was previously funded in a grant sponsored by Tian Medical.


mode network, salience network (SN) and central executive network (CEN) in chronic migraine (CM) with medication overuse headache (CMw/MOH).9 Fur-ther investigation of the node to node connectivity (NTNC) within the SN showed much more extensive disruption in regions involved in the mesocorticolimbic pathways bilaterally in CMw/MOH as compared to CM without MOH.10 This is similar to the findings of aber-rant mesocorticolimbic activity in CMw/MOH using task-based fMRI.11 The mesocorticolimbic system is rich in dopaminergic neurons and serves as neural sub-strate for pain, addiction, reward, and goal directed behavior. Disruption in this system has been linked to both migraine and overuse of pain medications.12-14


Given that that mesocorticolimbic system plays a large role in both the SN and CEN, it is plausible that exploration into these networks may prove use-ful in monitoring therapeutic outcome in this popula-tion. In theory, this method may not only be used as a biomarker, but also may provide insight into the mechanisms of SPG treatment. In this pilot study, we hypothesized that repetitive parasympathetic inhibi-tion via a series of SPG block would modulate rest-ing state NTNC within the SN and CEN, and that such neuromodulatory effect would involve mostly mesocorticolimbic regions in CMw/MOH.


Funding Source: McCausland Center for Brain Imaging (M-Fund) and University of South Carolina internal grant (ASPIRE II).




Participants.—Women were eligible for the study if they were at least 18 years old, met diagnostic




criteria fulfilling International Classification of Head-ache Disorders-III (beta)15 for CMw/MOH, had pre-dominantly frontal and/or orbital pain, and were eligible for receiving SPG blockade per manufac-turer’s instruction. Participants were excluded if they had cervicogenic headaches, or other headache treat-ment procedures such as nerve blocks or onabotuli-numtoxinA (Botox), physical therapy, or acupuncture six months before or during the treatment period. Furthermore, participants were excluded if they had MRI contraindication, neurological or pain disorders other than CMw/MOH, any chronic illness (ie, hyper-tension, diabetes, hepatic, renal, chronic inflamma-tory, or infectious disease, etc), unable to complete all SPG treatments within 6 weeks, or inability to follow study protocol while completing assessments. To min-imize any effect on functional BOLD (blood oxygena-tion level dependent) signal changes, participants with any possible confounding factors (ie, recreational drug use) were excluded.


All CMw/MOH participants were instructed to continue with the prophylactic medications, and use of acute pain medication as needed as usual with no new medications or headache related treatment started, throughout this 6 week period. All CMw/ MOH participants were age (6 5 years) and gender matched to healthy controls. Healthy controls were selected from a pool of healthy controls collected in a previous study.9,10 Controls were excluded if they had a family history of migraine or used over the counter/prescription pain medication for more than 5 days per month.


Each CM participant underwent 3 MRI scans:


(1)   immediately before their first SPG treatment, (2)


30 minutes after the initial treatment, and (3) 30 minutes after the last treatment of a series of 12 SPG blocks (twice per week). For the purposes of investi-gating the long term effect of a series of SPG treat-ment on neural networks, participants were scanned


30 minutes after the first treatment to account for any acute network connectivity changes. CMw/MOH participants were scanned at their baseline level of pain, at least 24 hours outside of their acute pain exacerbation period; any participant who came in within 24 hours of acute pain exacerbation was rescheduled.


May 2018



Clinical Parameters.—All participants underwent vital sign evaluations including a neurological exami-nation and completed a standardized questionnaire to ascertain clinical characteristics and demographic information (ie, age, sex, race, BMI, and educational level). The clinical characteristics included: (1) dura-tion of migraine history, (2) duration of CM history,


(3)    family history of migraine, (4) current medica-tions, (5) number of moderate to severe headache days per month, (6) location of migraine, (7) pres-


ence of aura, (8) headache-related disability as deter-mined by Headache Impact Test (HIT-6VR ),16 (9) depression as determined by Patient Health Ques-


tionnaire (PHQ-9),17 (10) allodynia as measured by allodynia symptom checklist (ASC 12).18


Standard Protocol Approvals, Registrations, and Participant Consent.—The study protocol was approved by the institutional review board at Uni-versity of South Carolina. Written informed consent was obtained from all participants.


Transnasal SPG Block.—In this study, all CMw/ MOH participants received a series of 12 SPG block-ade (twice per week for 6 weeks) using the Tx360VR (Tian Medical Inc; Lombard, IL, USA) with 0.5% bupivacaine. This device uses a small, flexible, soft plastic catheter to advance below the middle turbi-nate just past the sphenopalatine foramen. The plas-tic tube can then be rotated laterally on a preset track and extended into the intranasal cavity. A total of 0.3 mL of 0.5% bupivacaine is administered into each nostril over the mucosa covering the SPG.6,7 Dosing and anesthetic type was determined per device manufacturer’s recommendations.


MR Imaging Acquisition.—All participants were scanned on a Siemens 3T scanner located at the McCausland Center for Brain Imaging (Columbia, SC). Some participants (n 54) completed sets (before and after treatment) of scans prior to a sys-tem hardware (Trio to Prisma) upgrade; however, any variance due to this upgrade was controlled for in our analysis by adding this as a nuisance regres-sor variable to the general linear model using the Freedman-Lane approach.19 Participants were instructed to keep their eyes closed, stay awake, relax, and think of “nothing in particular” during the resting state scan. All conditions and lighting




were consistent throughout the entire study for all participants.


The imaging parameters for the Trio (12 channel head/neck coil) system consisted of a 6 minute high-resolution T1 weighted magnetization-prepared rapid gradient echo (MP-RAGE) scan (repetition time [TR] 52250 ms, echo time [TE] 54.15 ms, 192 slices, 50% slice gap, flip angle 598, voxel size 51.0 mm3, Field of View [FOV]5 256 mm 2, iPAT factor of 2, and using a sagittal, ascending, single shot acquisition) and a 15 minute resting state functional imaging scan using a T2* weighted BOLD contrast-sensitive sequence ([TR] 51550 ms, [TE] 534 ms, 42 slices, 20% slice gap, flip angle 5 718, voxel size 5 2.5 mm3, FOV5 215 mm2, and using a transversal, interleaved acquisition).


The imaging parameters for the Prisma (20 channel head/neck coil [16/4]) system included an acquisition of 6-minute high resolution T1 weighted MP-RAGE scan (same parameters as Trio except that TE 54.11 ms) and a 15-minute resting state functional imaging scan using a T2* weighted BOLD contrast-sensitive sequence (TR 5 1100 ms, TE 5 35ms, 56 slices, 20% slice gap, flip angle 5 728, voxel size 5 2.4 3 2.4 3 2.0 mm3, FOV5 216 mm2, and using a transversal, interleaved acquisition).


MR Imaging Processing.—Rs-fMRI preprocessing was completed using a combination of Statistical Parametric Mapping 12 software and custom Mat-lab scripts. The pipeline consisted of standard pro-cedures including motion correction, coregistration, normalization, frequency filtering (0.01 to 0.1 Hz band-pass), and spatial smoothing (8 mm full width at half maximum). For each network, a connectivity atlas was constructed using spherical (15 mm diam-eter) regions of interest (ROIs) centered on the peak Montreal Neurological Institute (MNI) coor-dinates for the a priori networks of SN and EN.20

The SN20 includes the bilateral dorsal anterior cingulate cortex (dACC), bilateral dorsolateral pre-frontal cortex (dlPFC), left anterior PFC (aPFC), bilateral hypothalamus, bilateral orbital frontal insula (OFI), paracingulate cortex, bilateral extended amygdala (EA), bilateral supramarginal gyrus (SMG), left periaqueductal gray, bilateral supplementary motor area (SMA)/pre SMA,





bilateral ventral tegmental area/substantia nigra (VTA/SNPC), bilateral superior temporal, bilateral temporal pole, bilateral ventral striatum/pallidum (vSP), and right ventrolateral PFC (vlPFC). The CEN20 consists of the bilateral anterior thalamus, bilateral dlPFC, bilateral dorsal PFC region of fron-tal eye fields (dPFC/FEF), bilateral vlPFC, dorsal medial PFC (dmPFC), right inferior frontal gyrus (IFG)/frontal operculum, right inferior temporal, bilateral lateral parietal, left OFI, bilateral dorsal caudate (dCaudate), and right ventromedial cau-date (vmCaudate). The exact ROIs (and their MNI coordinates) can be found in our previous publica-tion9,10 and are illustrated in Figure 1.


Statistical Analysis.—To create a functional con-nectivity matrix for each participant, the following steps were taken using MATLAB. First, we extracted the BOLD time series from each ROI (node) within a network (defined a priori).20 Then, for each network, a functional connectivity matrix was created by extracting the Fisher Z transformed Pearson’s correlation coefficient (r) for each pair of ROIs. The intranetwork connectivity strength (Table 1) is defined as the correlation coefficient (fisher Z transformed Pearson r value) generated for each pair of nodes within the network investi-gated. The overall connectivity strength of a net-work was derived by averaging all NTNC within each network.


We investigated the intranetwork NTNC in the SN (n 5 351) and CEN (n 5 136). For each network, a 2-tailed, paired sample t-test was used to evaluate difference in NTNC when comparing baseline to 30 minutes after first treatment, and baseline to 30 minutes after the last treatment (at 6 weeks; “End of Treatment [EOT]”). Each statistical test employed a permutation method, using 10,000 permutations, to control for multiple comparisons (using MAT-LAB).21 For each 9999 random permutations as well as the one actual ordering we logged the peak t-score for all regions (eg, maximum of 351 regions for SN). We then sorted these maximums and used the 500th most significant peak as our threshold to provide robust control for familywise error. These corrected P values of < .05 were considered significant for NTNC differences. No formal statistical test was

736                                                                                                                                                                                          May 2018





























































Fig. 1.—Axial and sagittal view of the salience (top) and central executive networks (bottom) as shown using the exact MNI coordinates. Images were made with “Surf Ice” ( Node depth is illustrated by transpar-ency with darker grey representing greater distance from the cortex.


Table 1.—Significantly Improved Intranetwork Nodal to Nodal Connectivity After Treatment

End of treatment

Salience network

Left aPFC 3 Left OFI
0.12 60.23
0.03 6 0.18
0.11 6 0.21
Left aPFC 3 Right OFI†
0.25 60.32
0.15 6 0.18
0.26 6 0.28
Left aPFC 3 Left vSP
0.21 60.18
0.02 6 0.19
0.14 6 0.19
Left aPFC 3 Right vSP†
0.26 60.22
0.05 6 0.17
0.22 6 0.19
Left aPFC 3 Right SMA/preSMA
0.37 60.31
0.25 6 0.25
0.32 6 0.3
Left aPFC 3 Right dlPFC
0.51 60.23
0.43 6 0.15
0.62 6 0.2
Left dlPFC 3 Right VTA/SNPC
0.05 60.15
20.1 6 0.12
0.03 6 0.17
Right Temporal Pole 3 Right VTA/SNPC
0.09 60.19
0.00 6 0.23
0.08 6 0.2
Left Superior Temporal 3 Right SMG
0.11 60.27
0.19 6 0.33
0.13 6 0.25
Central executive network

Left dlPFC 3 Left vlPFC
0.61 60.27
0.6 6 0.14
0.61 6 0.23
Left dlPFC 3 Right Anterior Thalamus†
0.28 60.17
0.17 6 0.11
0.27 6 0.16
Left dlPFC 3 Right vmCaudate
0.19 60.15
0.15 6 0.12
0.20 6 0.17
Left dlPFC 3 Right dPFC/FEF†
0.38 60.24
0.2 6 0.21
0.34 6 0.23
Left vlPFC 3 Right dPFC/FEF†
0.35 60.24
0.24 6 0.15
0.29 6 0.18
Left dPFC/FEF 3 Right Anterior Thalamus
0.21 60.17
0.03 6 0.17
0.18 6 0.17
Left dPFC/FEF 3 Right vmCaudate
0.16 60.12
0.00 6 0.14
0.04 6 0.14
Right dPFC/FEF 3 Right dCaudate
0.22 60.14
0.01 6 0.14
0.12 6 0.18


†Intranetwork connections that were also significantly different when comparing baseline to 30 minutes after the first treat-ment. Values represent mean 6standard deviation. The values listed in the “Controls” column are to illustrate what the “normal” connectivity strength is for the identified intranetwork connections (mean 6 standard deviation of 10 control sub-jects). The P values listed are comparing the baseline to end of treatment within the SPG group (paired sample). Abbreviations: aPFC, anterior PFC; dCaudate, dorsal caudate; dlPFC, dorsolateral prefrontal cortex; dPFC/FEF, dorsal PFC/ frontal eye field; OFI, orbital frontal insula; PFC, prefrontal cortex; SMG, supramarginal gyrus; SMA, supplementary motor area; VTA/SNPC, ventral tegmental area/substantia nigra; vSP, ventral striatum/pallidum; vlPFC, ventrolateral PFC; vmCau-date, ventromedial caudate.




used to compare the CM data with the control data, as the connectivity data for the controls were only used to visually demonstrate the normalization of the CM group after the SPG series.




Participants.—A total of 24 women (14 CM and 10 controls) were recruited between January 2015 and August 2016 from the University of South Carolina headache clinic (Columbia, SC). Four par-ticipants from the CM group were excluded due to the following reasons: motion artifact (n 51), scan-ner error (n 5 2), and unreported comorbid pain condition (n 5 1). Among the 10 participants, 8 had bilateral headaches, and 2 had left sided headaches. Individual characteristics for the CM group are summarized in Table 2. The control (n 5 10) partic-ipants were matched by age (41.9 6 11.5) and BMI (28.6 6 5.7).




Behavioral and Clinical Data.—Compared to baseline values, the number of moderate/severe headache days per month (P < .001), HIT-6 score (P < .001), PHQ-9 scored (P 5 .008) were all signifi-cantly improved at the EOT. Allodynia score was not significantly reduced at the EOT (P 5 .238). In addition to improved headache impact measure-ments, use of opioids (P 5.001), NSAID (P 5 .0016), and triptans (P 5 .003) were also significantly reduced at EOT. All behavioral data are summarized in Table 2 and specific medication used per partici-pant is summarized in Table 3.


fMRI Data.—When comparing baseline to EOT connectivity, several NTNC connections were signifi-cantly improved within the SN (n 59) and CEN (n 58) (Table 1, Fig. 2). Within the SN, improved con-nectivity was observed after treatment between the left aPFC to bilateral OFI and vSP, and contralateral SMA and dlPFC. Additionally, between right VTA/SNPC to


May 2018
Table 2.—Demographic and Clinical Features of Chronic Migraine With Medication Overuse Participants



28.5 6

10 females

43.3 6

8 Caucasian; 2 African American

Headache characteristics

End of treatment
Number moderate/severe headache days per month
21.1 6
11.2 6
Allodynia score

6.4 6
5.3 6
HIT-6 (headache impact test)

66.1 6
60.2 6
PHQ-9 (patient health questionnaire)

12.1 6
6.1 6
Medication use (days/month)

End of Treatment
Days of opioid use (n 5 7)

19.7 6
2.6 6
Days of NSAIDs use (n 5 7)

17.1 6
6.3 6
Days of triptan use (n 5 8)

14.5 6
6.5 6
Headache history

History of chronic migraine (years)

2.4 6

Family history (first degree)

n 5 8 (1 unknown)

History of migraine (years)

26.4 6


Values represent mean 6 standard deviation.




contralateral dlPFC and ipsilateral temporal pole. Lastly, a decrease in connectivity was observed between the left superior temporal and contralateral SMG; however, the trends suggest this still normalizes similar to the control data. Within the CEN, improved connectivity was observed between the left dlPFC to contralateral anterior thalamus, vmCaudate, dPFC/ FEF, and ipsilateral vlPFC, as well as between the left


dPFC/FEF to contralateral anterior thalamus and vmCaudate. Lastly, between right dPFC/FEF to ipsi-lateral dCaudate and contralateral vlPFC. We did observe improvement in the overall the connectivity (averages of all NTNC in a network) of the CEN (Baseline 0.00 60.08; 6 weeks 0.03 60.09, P 5 .01), but not the SN (Baseline 20.01 60.10; 6 weeks 0.01 60.12, P 5.26).



Table 3.—Reduction in the Use of Acute Pain Medications for Each Participant



Opioids or butalbital/month
NSAIDs/month (Baseline,
Triptans/month (Baseline,

(Baseline, during treatment,

during treatment, %

during treatment, %

% reduction)












Medication use was calculated by how many days in a month (30 days) the medication was used. Baseline use was determined in a period of 30 days before treatment and during treatment use was determined by the last 30 days of their treatment period.



Fig. 2.—Improved node to node intranetwork connectivity, unique to baseline vs end of treatment, within the salience network (top) and the central executive network (bottom) after a series of SPG blocks. [Color figure can be viewed at]





After recurrent parasympathetic inhibition via a series of SPG blocks, we have identified not only improved overall CEN connectivity, but also several intranetwork connections between regions of PFC (aPFC, dlPFC, vlPFC, and dPFC/FEF) and various limbic structures, as well as between different cortical regions. As CM is largely accompanied by pain and autonomic symptoms, variations in functional brain networks connectivity are thought to occur from the overwhelming need for the perception of pain and autonomic dysfunction. In normal pain modulation, increased activation of the aPFC, dlPFC, and vlPFC inhibit the painful stimuli from reaching the pain processing regions, contributing to an analgesic effect.22-24 These key prefrontal regions, vital to the cognitive (top down pain modulation) aspect of pain processing and relevant saliency (bottom up filtration) of pain modulation, have been found to be dysregu-lated in CMw/MOH patients.9,10,25 Interestingly, con-nectivity between many of these dysregulated regions in both networks exhibit a marked improvement after as series of SPG treatments.


Salience Network.—Our result suggests that the function of the SN, regardless of increased or decreased connectivity (synchronization) at baseline in CMMOH, were partially restored to a normal state after treatment. Specifically, we noted near complete recovery of connectivity between the left aPFC, and various cortical and limbic regions (OFI, VTA/SNPC, and vSP) within SN. It is possible that recurrent SPG inhibition modified these connectivi-ties, given the relative close proximity of SPG to aPFC and the importance of left PFC in parasym-pathetic function.26 Interestingly, midbrain dopa-mine neurons (including VTA and SNPC) are the key regions of the reward network, and disruptions in these regions are implicated in overuse of pain medications.27,28 Therefore, the improved synchro-nization between these regions may result in the decreased desire for taking acute pain medications, which is evident by the significant reduction in acute pain medication usage in our participants (Tables 2 and 3). Despite these subjectively near normalized NTNC, we did not observe improve-ment of overall SN connectivity. Clinically, this


May 2018



may explain why the allodynia score was not signifi-cantly lower in our participants after treatment, given that this network connectivity is correlated with changes in allodynia score.9 Our data suggest that repetitive SPG inhibition may help to reduce the saliency of pain by partially reversing the aber-rant cortical and subcortical connectivity within the mesocorticolimbic system in these patients.


Central Executive Network.—Within the CEN, improved connectivity was observed in overall con-nectivity strength and between regions of the PFC and cortico-thalamic-striatal regions. Cognitive con-trol in pain modulation is diverted to “pain-reduction-related processes” in CM.29 As many of these PFC regions within the CEN are also involved in pain modulation pathways, it is likely that these disruptions in the CEN are related to constant “hijacking” of cognitive resources. The improved connectivity of several frontal cortex regions were demonstrated in our participants, and may be reflective of a lessening of burden on these cognitive resources. Taken together, these findings further support the hypothesis that recurrent para-sympathetic inhibition is associated with improved functional connectivity in brain regions critical to pain processing in CMw/MOH.



Left Prefrontal Cortex.—Across both networks we found that the majority of the PFC regions that recovered after treatment are in the left hemi-sphere. Locations of the headaches in our patients do not seem to have any impact on this, as 80% of them had bilateral headaches. The autonomic con-trol in the central nervous system is maintained through homeostatic balance between the left (parasympathetic) and right PFC (sympathetic).26 As SPG blockade is most likely to affect parasym-pathetic outflow, this may explain why left PFC regions appear to improve more after treatment. We postulate that repetitive parasympathetic inhibi-tion via SPG may restore the homeostatic balance by predominantly improving parasympathetic tone in the left PFC.



Limitations.—We do acknowledge there are limi-tations of this pilot study. First, the sample size is small; however, we were able to reach sufficient sta-tistical power using a longitudinal, within the group




comparison design. Future studies would benefit from increased sample size, and scanning healthy controls at the same time point intervals to control for any longitudinal brain connectivity changes. Second, it is possible that the improved connectivity may be partially related to the placebo effect. To control for this, we examined common improve-ments, seen in the analysis of baseline vs 30 minutes after first treatment and baseline vs EOT, to highlight any similarly improved nodes. These nodes that showed improved connectivity have been previously implicated in placebo analgesia30 and may be associated with immediate pain reduc-tion or “anticipation of pain relief.” Ideally, a dou-ble blinded placebo controlled methodology could have been employed. However, as a pilot study, the purpose was not to evaluate the efficacy of SPG in CMw/MOH, but rather to investigate the longitudinal intrinsic functional brain network connectivity changes associated with this treatment.


Another possible confounder is the reduction of acute pain medication usage which occurred in all of our patients, likely due to reduced headache fre-quency (Table 3). For ethical reasons, use of acute pain medication could not be maintained. However, given significant reduction of migraine days in these patients, a possible explanation is that successful detoxification with the treatment modified the risk factor for CMw/MOH. Despite this, we still think a larger cohort study to investigate the confounding effects of acute medications on resting state connec-tivity using a multivariate linear regression model may be helpful to address this issue. Additionally, we cannot be certain that our findings are a consequence of SPG inhibition or if they are causal, as we are unable to determine if these changes in connectivity are due to reduced headache/migraine or if is a response to a general reduction of chronic pain. This question maybe better answered using a cohort group of another chronic pain disorder. Currently, there is no technique to definitively confirm that only SPG was targeted by the local anesthesia using intra-nasal approach, other nearby structures such as max-illary branch of trigeminal nerve may have been affected by the treatment.






Despite incomplete normalization of the func-tional brain networks, our results suggest that recurrent parasympathetic inhibition via a series of SPG blocks is associated with long term neuromo-dulatory effect in CMw/MOH. We postulate that repetitive SPG inhibition may modulate the activ-ity of various neuropeptides within the ganglion, resulting in improved resting state intrinsic func-tional connectivity, especially the left PFC, likely through decreased parasympathetic outflow to cra-nial and meningeal vessels. Furthermore, it may modulate resting state functional connectivity in mesocorticolimbic regions, likely through the con-nection between SPG to SSN.31 These bidirec-tional effects originating from the recurrent SPG inhibition extracranially may subsequently lead to partial restoration of the affected connectivity changes associated with CMw/MOH. Future study with a large sample size is needed to further unravel the neurobiological basis underlying the role of SPG in CMw/MOH.






Category 1


(a)   Conception and Design


X.    Michelle Androulakis, Kaitlin Krebs


(b)    Acquisition of Data


X.    Michelle Androulakis, Kaitlin Krebs


(c)    Analysis and Interpretation of Data


X.    Michelle Androulakis, Kaitlin Krebs, Chris Rorden


Category 2


(a)   Drafting the Manuscript


X.    Michelle Androulakis, Kaitlin Krebs


(b)    Revising It for Intellectual Content


X.    Michelle Androulakis, Kaitlin Krebs, Chris Rorden


Category 3


(a)   Final Approval of the Completed Manuscript X. Michelle Androulakis, Kaitlin Krebs, Chris Rorden





1.  Khan S, Schoenen J, Ashina M. Sphenopalatine ganglion neuromodulation in migraine: What is the rationale? Cephalalgia. 2014;34:382-391.


2.  Robbins MS, Robertson CE, Kaplan E, et al. The sphenopalatine ganglion: Anatomy, pathophysiol-ogy, and therapeutic targeting in headache. Head-ache. 2016;56:240-258.


3.  Goadsby PJ, Lipton RB, Ferrari MD. Migraine— current understanding and treatment. N Engl J Med. 2002;346:257-270.


4.  Moskowitz MA. Basic mechanisms in vascular headache. Neurol Clin. 1990;8:801-815.


5.  Maizels M, Aurora S, Heinricher M. Beyond neu-rovascular: Migraine as a dysfunctional neurolim-bic pain network. Headache. 2012;52:1553-1565.


6.  Cady R, Saper J, Dexter K, Manley HR. A double-blind, placebo-controlled study of repeti-


tive transnasal sphenopalatine ganglion blockade with Tx360VR as acute treatment for chronic migraine. Headache. 2015;55:101-116.


7.  Cady RK, Saper J, Dexter K, Cady RJ, Manley HR. Long-term efficacy of a double-blind, pla-cebo-controlled, randomized study for repetitive


sphenopalatine blockade with bupivacaine vs saline with the Tx360VR device for treatment of chronic migraine. Headache. 2015;55:529-542.


8.  Yarnitsky D, Goor-aryeh I, Bajwa Z, et al. Possi-ble parasympathetic contributions to peripheral and central sensitization during migraine. Head-ache. 2003;43:704-715.


9.  Androulakis XM, Krebs K, Peterlin BL, et al. Modula-tion of intrinsic resting-state fMRI networks in women with chronic migraine. Neurology. 2017;10-212.


10.  Androulakis XM, Rorden C, Peterlin BL, Krebs KA. Modulation of salience network intranetwork resting state functional connectivity in women with chronic migraine. Cephalalgia. 2018; Accepted.


11.  Ferraro S, Grazzi L, Mandelli ML, et al. Pain processing in medication overuse headache: A functional magnetic resonance imaging (fMRI) study. Pain Med. 2012;13:255-262.


12.  Cahill CM, Cook C, Pickens S. Migraine and reward system—or is it aversive? Curr Pain Head-ache Rep. 2014;18:410.


13.  Koob GF, Volkow ND. Neurocircuitry of addic-tion. Neuropsychopharmacology. 2010;35:217-238.


14.  Jasinska AJ, Stein EA, Kaiser J, Naumer MJ, Yalachkov Y. Factors modulating neural reactivity


May 2018



to drug cues in addiction: A survey of human neu-roimaging studies. Neurosci Biobehav Rev. 2014; 38:1-6.


15.  The International Classification of Headache Disor-ders, 3rd edition (beta version). Headache Classifi-cation Committee of the International Headache Society (IHS). Cephalalgia. 2013;33(9):629-808.


16.  Shin HE, Park JW, Kim YI, Lee KS. Headache Impact Test-6 (HIT-6) scores for migraine patients: Their relation to disability as measured from a headache diary. J Clin Neurol. 2008;4:158-163.


17.  Seo JG, Park SP. Validation of the Patient Health Questionnaire-9 (PHQ-9) and PHQ-2 in patients with migraine. J Headache Pain. 2015;16:65.


18.  Lipton RB, Bigal ME, Ashina S, et al. Cutaneous allodynia in the migraine population. Ann Neurol. 2008;63:148-158.


19.  Freedman D, Lane D. A nonstochastic interpreta-tion of reported significance levels. J Bus Econ Stat. 1983;1:292-298.


20.  Seeley WW, Menon V, Schatzberg AF, et al. Disso-ciable intrinsic connectivity networks for salience processing and executive control. J Neurosci. 2007; 27:2349-2356.


21.  Winkler AM, Ridgway GR, Webster MA, Smith SM, Nichols TE. Permutation inference for the gen-eral linear model. Neuroimage. 2014;92:381-397.


22.  Lorenz J, Minoshima S, Casey KL. Keeping pain out of mind: The role of the dorsolateral prefron-tal cortex in pain modulation. Brain. 2003;126: 1079-1091.


23.  Salomons TV, Johnstone T, Backonja MM, Shackman AJ, Davidson RJ. Individual differences in the effects of perceived controllability on pain perception: Critical role of the prefrontal cortex. J Cogn Neurosci. 2007;19:993-1003.


24.  Wiech K, Kalisch R, Weiskopf N, et al. Anterolat-eral prefrontal cortex mediates the analgesic effect


of  expected  and  perceived  control  over  pain.


J Neurosci. 2006;26:11501-11509.


25.  Bingel U, Tracey I. Imaging CNS modulation of pain in humans. Physiology. 2008;23:371-380.


26.  Hilz MJ, Dutsch€ M, Perrine K, et al. Hemispheric influence on autonomic modulation and baroreflex sensitivity. Ann Neurol. 2001;49:575-584.


27.  Kuhnen CM, Knutson B. The neural basis of financial risk taking. Neuron. 2005;47:763-770.


28.  Corlett PR, Aitken MR, Dickinson A, et al. Pre-diction error during retrospective revaluation of




causal associations in humans: fMRI evidence in favor of an associative model of learning. Neuron. 2004;44:877-888.


29.  Mathur VA, Khan SA, Keaser ML, et al. Altered cognition-related brain activity and interactions with acute pain in migraine. Neuroimage Clin. 2015;7:347-358.




30.  Wager TD, Rilling JK, Smith EE, et al. Pla-cebo-induced changes in FMRI in the anticipa-tion and experience of pain. Science. 2004;303: 1162-1167.


31.  Akerman S, Holland PR, Goadsby PJ. Dience-phalic and brainstem mechanisms in migraine. Nat Rev Neurosci. 2011;12:570-584.

Acupuncture for Migraines

May 22, 2018 Uncategorized 0 Comments

Acupuncture for Migraines

Acupuncture is one of the oldest medical techniques in the world, practiced in China for over 2,000 years. It is a FDA-approved treatment modality for a number of illnesses, especially pain management and chronic pain, and is particularly effective in treating migraines.

Acupuncture is a Traditional Chinese Medicine treatment that involves stimulating some of the over 800 vital energy points in the human body with fine, hair-thin needles to release chi and encourage the body to heal itself. The vital energy points are on the meridians that run through the body from head to toe.

Chi (pronounced chee), or life energy, flows through these meridians and energy points.
The obstruction of the flow of chi leads to illness and is considered the source of many bodily aches and pains. The flow of chi along the meridians can be obstructed by illness, poor diet, the weather, and other outside factors.

Most acupuncture practitioners work with patients to form a treatment plan that addresses both the blockages themselves and the things that cause them. These treatment plans, like those of Western Medicine, often include diet and lifestyle changes to enhance the patients’ well-being.

Migraineurs (people who suffer from migraine headaches) need to tell their acupuncturist exactly where they hurt when seeing one for pain mitigation. The location of pain is important due to the large number of acupuncture points in the head, face, and neck. Where to apply pressure depends on where the migraine pain is most acute.

Migraineurs can find long-term relief from their migraines by working with an acupuncturist who specializes in headaches. These specialists do an individualized assessment of the patient to create a long-term treatment plan. Many people who undergo an acupuncture program like this experience relief from migraines for years afterward. For some the headaches stop completely.

Pressure Points To Relieve Headaches

May 20, 2018 Uncategorized 0 Comments

Pressure Points To Relieve Headaches

Medication isn’t always the best option for getting rid of headache pain. Sometimes you won’t have the pain reliever on hand, other times it won’t work, and there is also the possibility that you don’t like the idea of using drugs to treat your ailments. Pressure points to relieve headaches let you get rid of the pain without relying on drugs.

It’s not entirely understood how these pressure points work, but that doesn’t matter. The only thing you care about is that they can work. While they won’t always bring the relief you need, they work often enough to be useful. The best part is that they are a completely natural alternative to medicinal pain relievers.

If your headaches are not easily controlled, are new, or are stronger than usual, then see your doctor. While the chances are small, it’s possible that you have a much more serious condition that requires professional medical attention. Also, this article is not meant to be taken as medical advice of any kind; you can only get that from a qualified doctor.

Here are a few of the best pressure points to relieve headaches:

1. Your temples – Use two fingers from each hand and make a gentle, circular motion. Don’t press too hard, as the temples can be sensitive. Try doing this for 30 to 60 seconds, and then take a short break before doing it again.

2. The bridge of your nose – At the inside of the top of your nose where your eyebrows meet are some very effective pressure points. Simply massage the area with your fingers, applying a fair amount of pressure.

3. Your hairline – To be precise, the pressure points run along the front portion of where the hairline should be. If you have a receding hairline or are bald then you need to imagine where the hairline is. A circular massaging motion using the heel of your hand should help to ease the pain of most types of headaches.

4. Between your index finger and thumb – Here you will find a fold of skin. Pinch it firmly and then rub it. Do this for 30 to 60 seconds on one hand, and then switch to the other. You can also try using some padding and a clothespin, though that can be a bit painful for some people.

5. The shoulder blades – Most people tend to go right for the tops of the shoulders, and that can help, but one of the best pressure points to relieve headaches is found: approximately one-half of the distance between your head and the outside of your shoulders.

Using pressure points to relieve headaches means that you don’t have to rely on medication or questionable treatments ever again. Instead, you can simply use your favorite pressure point whenever the pain in your head starts, and massage your way to relief. You will always have a way of treating headaches, no matter where you go.