Alcohol overuse has been associated with new daily persistent headache. On occasion, alcohol is used in an attempt to dull pain. This is not a good practice for a number of reasons, but it’s certainly not a great idea if it ends up giving you a chronic headache. This does not, of course, mean an occasional hangover headache, but is referring to general alcohol overuse and problem drinking.
What are the reasons headache sufferers might abuse alcohol? Is alcohol use associated with anxiety disorders? There is actually some evidence to suggest that alcohol dependence may be twice as high in people with anxiety disorders as in the general population.
Watch for these symptoms of a drinking problem:
More than three drinks per day or more than 7 drinks per week if you are a woman (or a man over age 65)
More than four drinks per day or more than 14 drinks per week if you are a man (under age 65)
Inability to stop drinking at a given time (binge drinking)
Failure to do what was expected of you because of drinking
“Blackouts” or memory loss because of drinking, like forgetting what happened the night before
Needing a drink first thing in the morning
Losing friends because of drinking
Feeling guilty about how much you drink
Feeling annoyed or angry when people talk about how much you drink, or when you read things like this list
If you think you might have a problem, talk to someone. Seek help for your problem drinking. Be smart, and get control of your drinking. And don’t use headache as an excuse to drink, because it’s not really a very good one. Who wants a daily headache?
While there has been a recognized association between bruxism (grinding) and temporomandibular disorders, this has not been well-studied with respect to headache disorders. One study found that 40% of patients presenting with TMD also had migraine. The authors of the study note that further research is necessary.
Clenching has been associated with anxiety disorders, and may be highly comorbid with migraine as well. Although formal studies of temporomandibular dysfunction in migraine are lacking, many headache experts note a correlation between TMD symptoms in their migraine patients.
Types of Temporomandibular Dysfunction
The American Academy of Orofacial Pain recognizes two types of temporomandibular dysfunction. These are called myogenous (related to muscles) and arthrogenous (related to joints). Myogenous TMD is due to bruxism, clenching, or both, and has no evidence of joint issues. Arthrogenous TMD is due to problems with the jaw joint itself, and may include degeneration of the disc in the jaw joint. Many people with TMD will have both types.
TMD occurs more frequently in women, with a 4:1 ratio reported. Not everyone with TMD is depressed. Some people with TMD have abnormalities in a gene called serotonin transporter gene, which has also been found in association with depression. Serotonin transporter gene changes have also been associated with the emotional processing of pain, and may cause an increase in migraine attacks as well as TMD pain.
Symptoms of arthrogenous TMD are popping or clicking of the jaw, inability to fully open the jaw, ear pain or a sense of fullness in the ear, ringing of the ear, dizziness, and hyperacusis (hypersensitivity to normal sound levels). Myogenous TMD causes pain in the jaw and muscles of the face.
Treatment of Tempormandibular Dysfunction
The TMJ Association recommends the following self-management measures for TMD: moist heat, cold packs, at least temporary avoidance of hard or chewy foods, or foods that make you open your jaw wide, like apples or corn on the cob, and good general dental care. In addition to maintaining a good posture in general, you should avoid sitting with your chin in your hand, and you should not sleep on your stomach. Also keep in mind the saying, “lips together, teeth apart.”
These measures are not a substitute for medical or dental evaluation. If they are minimally helpful, you may require physical therapy or dental treatment, which can include an oral device.Your physician or dentist will be able to determine whether you need referral to an oral surgeon or craniofacial specialist.
There is little evidence that either orthodontia or occlusal adjustment can prevent or treat temporomandibular dysfunction, according to the Cochrane Summaries.
References:
1. Palit S, Sheaff RJ, France CR, et al. Serotonin transporter gene (5-HTTLPR) polymorphisms are associated with emotional modulation of pain but not emotional modulation of spinal nociception. Biol Psychol. 2011;86(3):360-369.
2. Kotani K, Shimomura T, Shimomura F, Ikawa S, Nanba E. A Polymorphism in the Serotonin Transporter Gene Regulatory Region and Frequency of Migraine Attacks. Headache: The Journal of Head and Face Pain. 2002;42(9):893-895.
3. Esposito, CJ, Fanucci, PJ, Farman, AG. Associations in 425 patients having temporomandibular disorders. J Ky Med Assoc. 2000;98(5):213-215.
4. Gatchel, RJ, Stowell, AW, Buschang, P. The relationship among depression, pain, masticatory functioning in temporomandibular disorder patients. J Orofacial Pain. 2006;20(4):288-296.
5. Ojima, K, Watanabe, N, Narita, N, Narita, M. Temporomandibular disorder is associated with a serotonin transporter gene polymorphism in the Japanese population. Biopsychosoc Med. 2007;1:3. pub online 2007, Jan 10, doi: 10.1186/1751-0759-1-3.
6. Luther F, Layton S, McDonald F. Orthodontics for treating temporomandibular joint (TMJ) disorders. In: The Cochrane Collaboration, McDonald F, eds. Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons, Ltd; 2010. Available at: http://summaries.cochrane.org/CD006541/orthodontics-for-treating-temporomandibular-joint-tmj-disorders. Accessed January 10, 2012.
7. Koh H, Robinson P. Occlusal adjustment for treating and preventing temporomandibular joint disorders. In: The Cochrane Collaboration, Koh H, eds. Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons, Ltd; 2003. Available at: http://summaries.cochrane.org/CD003812/occlusal-adjustment-for-treating-and-preventing-temporomandibular-joint-disorders. Accessed January 10, 2012.
While there has been a recognized association between bruxism (grinding) and temporomandibular disorders, this has not been well-studied.
Clenching has been associated with anxiety disorders, and may be highly comorbid with migraine as well. The trigeminal nerve, which is associated with migraine, also innervates the masseter muscle, which is the muscle responsible for clenching the jaw. It is felt by many headache experts that activation of the trigeminal nerve—which happens in migraine—will result in activation of the masseter muscles during a migraine.
Awake bruxism – clenching during the day – is present in about 20% of the population, and is usually stress-related. Bruxism at night affects about 8% of the population, and has been classified as a sleep-related movement disorder.
Clenching is also a possible adverse effect of the SSRI antidepressants.
Clenching, grinding, or temporomandibular dysfunction (TMD) can trigger any type of headache, or make it worse.
If you have a tendency toward clenching, awareness of the condition can help you reduce clenching. Physical therapy and relaxation training can be helpful. If you have a tendency toward clenching or grinding, you should avoid chewing gum. Some people may benefit from an oral device. Read more about that in TMD/TMJ.
1. Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K. Bruxism physiology and pathology: an overview for clinicians. Journal of Oral Rehabilitation. 2008;35(7):476-494.
Guest post by Dr. Ingo Anderle, ophthalmic optician
There is a correlation between headaches and migraines and improperly corrected refractive errors and undetected strabismus. This indicates a need to build closer interprofessional relationships between neurology and optometry
This article serves to illustrate the experience I have had with headache patients in my optometric and optical practice, the effects of detecting improper correction of refractive errors, and the detection of hidden strabismus. The correction of these problems results in patients seeing better, having a better life, and having found relief.
To emphasize the need for a closer collaboration between neurology and optometry, I will use two cases I have seen at my practice and treated accordingly.
CASE I
Female patient, 42 years of age, wearing glasses for close to 35 years. Myopic (near-sighted), with astigmatism and anisometropia of 2dpt.
Patient comes in for a check-up to get new glasses. Her history reveals that she has been suffering almost daily from headaches since puberty and increasingly from migraines, which at the time of consultation averaged 3 days per week. Consulting a number of doctors about her migraines and headaches did not provide effective treatment and left her with medication to be taken as required. Patient is working in an office environment, spending about 8 hours on a computer. Hobbies include knitting and other close range activities and the use of a laptop computer at home.
Initial exam reveals her current Rx (2 years old) is over-minussed with 1dpt OS, overall, slight changes in prescribed correction for astigmatism. Fundus eye exam is normal, anterior part doesn’t show any pathologies.
During binocular testing, the patient was shown a split screen red/green image and trial frames fitted accordingly with red and green filter. The patient was asked to describe what she sees and reported that the clarity of image was identical, but that the left hand side green image kept wandering over to the left. This procedure, as well as the way the question was posed, revealed the strabismus and the need of 5pdpt, Base 0º of correction OS. Had the patient only been asked which side was better, rather than to describe her experience, she would have answered they were identical and that would have left the strabismus undiagnosed. Accomodation is still fine for near vision and only long distance Rx is prescribed.
(New Rx OD: -3.00(cyl -0,50 x5º) / OS: -5,75 (cyl -0,50 x75º) P 5pdpt Base 0º)
Glasses were made at our in-house workshop. Prism is fitted only OS. (Lenses used: Zeiss Clarlet 1.67 Aspheric with Lotutec AR.) Centres are fitted at 3mm below pupil centre and at exactly the same I.P.D. as in the trial frames during the eye exam. After wearing the glasses with the new Rx for only 3 days the patient is reporting a significant improvement in visual acuity and not suffering from headaches as before.
At the annual check-up the patient reported an almost complete cessation of headaches and only occasionally suffering from a migraine (usually weather dependent). Vision Rx is stable and reading glasses with Add 1.00 are prescribed.
At the 2 year check-up the patient is reporting the same as the year before, Rx is stable and reading Add has changed to 1.25. The patient requested seperate reading glasses. Prism is fitted at 4pdpt and patient is reporting her satisfaction with her new glasses.
CASE II
Female patient, 35 years of age turns up for a new Rx for new glasses. Medical history reveals that the patient is suffering from moderate to severe headaches over a period of 5 years. The average daily medication taken is Ibuprofen 1200mg or equivalent in Paracetamol (acetaminophen). Her current glasses are of the following RX: OD -4.00 (cyl -0,75 x 25º) P 1,5pdpt Base 270 (vertical prism) OS: -2,00 (cyl -1,00 x 5º). The glasses appeared to be very tilted and not in a straight position on the patients face. When mentioned this, she said “I see better that way.”
Over the past 5 years the patient underwent a number of exams and consulted a neurologist numerous times. An MRI and CT scan were performed, both normal. The patient was at the point of giving up trying to find a cure for the headaches and was trying to live with them and not expecting any improvement.
The exam revealed the following RX: OD -3.00 (cyl -0,50 x30º) /OS: -2,00 (cyl-0,75 x 175º), no vertical prism was detected, and again overminussed OD.The vertical prism in her glasses must have been caused by a mistake during the fitting process of the lenses, since no vertical prism was detected during the exam. Her problems with headaches started soon after she had the current pair of glasses made and since then she did not have an eye exam and no new glasses.
The patient did not want to believe that just a new Rx and new glasses would make a significant difference in regard to her headaches. Understandably, after a 5 year ordeal, MRI and CT scans, and consulting neurologists, she did not have any confidence in finding a cure.
However, new glasses were made and after only 2 days she reported back and could not believe that she had not had a headache and that she was generally feeling a lot better. Two weeks later, I called for a follow up and she reported a continued absence of headaches and came in to order a second pair of glasses.
CONCLUSION
As both cases illustrate, there can be a lack of good quality service available when it comes to eye examinations, and there is a shortfall in interprofessional collaboration between neurology and optometry.
Both patients would have benefitted greatly from being referred to an optometrist by their doctors, but both patients also had the unlucky experience with incorrect prescriptions and/or incorrectly made glasses and a lack of experience in binocular testing.
Current practice here in Andalucia (southern Spain) is that a doctor (mostly the GP) refers patients with symptoms such as headaches and blurred vision to consult an optometrist IF they currently do not wear glasses. If a patient is wearing glasses, it is widely assumed that they must be correct (both regarding Rx and correctly fitted) and I hardly ever see a referral to an optometrist.
The relationship between wrongly corrected eyesight or undercorrection and headaches is known and nothing new.
In my opinion it would be good to see more referrals from neurologists to the optometrist, even if it is to exclude wrongly/undercorrected eyesight in the diagnostic process.
POINTERS FOR THE OPTOMETRIC PROFESSION
There is a large shortfall in the quality of eye examinations by ophthalmologists and optometrists, especially in the way they conduct the pre-examination medical history (neither age, nor medications taken, underlying health conditions not explored, workplace and hobbies that give an idea on the demand the patient will have on vision and glasses not identified). Also, during the exam itself, leading questions do not assist in getting the correct picture. If the only question asked is whether one or the other option is better or worse, it does not allow the patients to accurately describe the visual picture they actually see. After all, the issued Rx is a subjective Rx.
Dr. Anderle is an optometrist practicing in southern Spain.
In a small study of children with migraine (109 children six and over) the presence or absence of a heart defect known as patent foramen ovale was studied. Thirty-five per cent of the children in the study had migraine with aura. About half of the migraine with aura kids had the PFO heart defect, as compared to 27% of the children with migraine without aura.
What is PFO?
PFO (patent foramen ovale) is a form of heart defect. The foramen ovale is a hole in the heart wall that has a purpose when a baby is in the womb. It allows blood to bypass the lungs, because babies do not breathe with their lungs until they are born, and get their oxygen from the mother’s blood. Once born, this opening usually closes naturally in infants. Sometimes when it persists past infancy, a PFO will still close spontaneously, but this generally occurs before age six.
In the adult migraine population, it has been found that about 25% of all migraine patients have PFO. Trials of PFO closure in adults have been inconclusive. Several smaller, single center trials have shown high response rates to closure of PFO. The only multi-center, double-blind trial of PFO closure failed to show positive results, but was potentially flawed in terms of patient selection and other technical issues.
In this study, the severity of migraine was not associated with the presence or absence of PFO. The study was limited by the inability to place IV lines in control subjects and do a direct comparison of data from the study population and the control population. Because of the small sample size in this study and because of the other controversies associated with testing and treatment of PFO, authorities in the field have recommended further study before recommending PFO closure in children.
Is there a correlation between high blood pressure and migraine? Maybe. There have been studies to suggest that uncontrolled hypertension (high blood pressure) may result in an increase in migraine headache frequency or severity. However, it has also been argued that since both high blood pressure and migraine are commonly occurring conditions, any such relationship is mere coincidence.
Certainly, there can be transient increases in blood pressure during a headache of any type, simply because you are in pain, so it stands to reason that chronic headache sufferers might experience higher overall blood pressure.
Can high blood pressure cause a headache? Usually this is not the case unless blood pressure is extremely high.
A recent retrospective epidemiological study, which means it was looking back in time at previously collected data, actually proposed that maybe hypertension even protects against headache! Other studies, however, seem to suggest that there might be a correlation between hypertension and the transition from episodic to chronic migraine. It has even been suggested that there may be a protective effect for systolic blood pressure (the top number), but a negative effect for diastolic blood pressure (the bottom number).
The MIRACLES Study, also known as Hypertension and Migraine Comorbidity: Prevalence of Cerebrovascular Events, looked at 2973 patients with hypertension, migraine, or both. About 17% of the subjects had both hypertension and migraine, 40% had migraine only, and 43% had hypertension only. In the subjects with both conditions, migraine onset was older than in the migraine-only group, and onset of hypertension was earlier than in the hypertension-only group. Hypertension was harder to control, and there was often a family history of both migraine and hypertension.
The group with migraine-hypertension comorbidity had a 4.4% risk of stroke, as compared to 3.1% in the hypertension-only group, and 0.7% in those with migraine only. In the 40-49 year-old age group, the rate of previous stroke (or TIA) in the group with both conditions was five times higher than in the hypertension-only group.
It is thus likely that there is a migraine-hypertension link in some migraine patients that may be genetically based. Clearly, more studies are required so that we can understand this connection better.
References:
1. Hagen K, Strovmer LJ, Vatten L, et al. Blood pressure and risk of headache: a prospective study of 22 685 adults in Norway. J Neurol Neurosurg Psychiatry 2002;72:463–6.
2. Friedman, D. Headache and hypertension: refuting the myth. J Neurol Neurosurg Psychiatry 2002;72:431.
3. Bigal ME, Sheftell FD, Rapoport AM, Tepper SJ, Lipton RB. Chronic Daily Headache: Identification of Factors Associated With Induction and Transformation. Headache: The Journal of Head and Face Pain. 2002;42(7):575-581.
4. Agostoni E, Aliprandi A. Migraine and hypertension. Neurol Sci. 2008;29(S1):37-39.
5. Mancia G, Agabiti-Rosei E, Ambrosioni E, et al. Hypertension and migraine comorbidity: Prevalence and risk of cerebrovascular events. Evidence from a large, multicenter, cross-sectional survey in Italy (MIRACLES study). J Hypertens 2011; 29:309–318.
Recent Comments