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Discussion paper prepared for
The Workplace Safety and Insurance Appeals Tribunal
Dr. John Edmeads
Professor of Medicine (Neurology)
University of Toronto
Dr. John Edmeads graduated from the Faculty of Medicine of the University of Toronto in 1959. He pursued post-graduate studies in neurology and became a Fellow of the Royal College of Physicians and Surgeons in 1965. He served the College as Chief Examiner in neurology from 1981 to 1983. He joined the University of Toronto faculty in 1967 and became Professor of Medicine in 1984. He led research in cerebral blood flow, chronic headache and medical education. He received numerous awards for his work and teaching in these areas. Dr. Edmeads was Head of Neurology at Sunnybrook Health Science Center from 1969 to 1993 and Head of the Department of Medicine and Physician in Chief at Sunnybrook Health Science Center from 1994 to 2001. Dr. Edmeads died in April 2007.
WSIAT literature search reviewed by Dr. D. Rowed in 2010, who is of the opinion that this paper still provides a balanced overview of the medical knowledge in this area.
This medical discussion paper will be useful to those seeking general information about the medical issue involved. It is intended to provide a broad and general overview of a medical topic that is frequently considered in Tribunal appeals.
Each medical discussion paper is written by a recognized expert in the field, who has been recommended by the Tribunal’s medical counsellors. Each author is asked to present a balanced view of the current medical knowledge on the topic. Discussion papers are not peer reviewed. They are written to be understood by lay individuals.
Discussion papers do not necessarily represent the views of the Tribunal. A vice-chair or panel may consider and rely on the medical information provided in the discussion paper, but the Tribunal is not bound by an opinion expressed in a discussion paper in any particular case. Every Tribunal decision must be based on the facts of the particular appeal. Tribunal adjudicators recognize that It is always open to the parties to an appeal to rely on or to distinguish a medical discussion paper, and to challenge it with alternative evidence: see Kamara v. Ontario (Workplace Safety and Insurance Appeals Tribunal)  O.J. No. 2080 (Ont Div Court).
Headache is not a disease. It is a symptom, with many causes, mostly benign (like migraine) and rarely ominous (like brain tumor). This discussion will focus on headaches encountered in the setting of the workplace - headaches associated with traumatic injury to the head and/or neck, and headaches related to exposure to toxic substances.
As prologue, it is important to become familiar with the causes of headaches in general, and with the benign dysfunctional headaches (such as migraine and tension-type headaches) that so many people have as a result of hereditary, stress, or idiopathic (ie unknown) factors.
Headaches occur when pain-sensitive structures in the head (and sometimes neck) are disturbed by malfunction or disease. The pain-sensitive structures of the head and neck, and the things that may irritate them, are shown in the table. Note that the brain tissue itself is not sensitive to pain, but its coverings (the meninges) and the blood vessels that supply it, are. The coverings of the skull (scalp tissue, muscle, nerves and blood vessels), the eyes, the sinuses, the teeth, and the jaw joints, are all sensitive to pain.
|Structure||Stimulus||Type of Headache (h/a)|
|Scalp & neck muscles
Post-traumatic tension h/a's
Site of injury head pains
|Joints & ligaments of neck||Traumatic injury||"Whiplash headaches"|
|Blood vessels of scalp||Idiopathic* dilatation||Migraine headaches|
|Blood vessels inside head||Idiopathic* dilatation
Brain tumor, hematoma
|Coverings of brain (meninges)||Infection
Inflammation (by blood)
Bleeding into brain
|Nasal sinuses||Infection, inflammation||Headaches of sinusitis|
|Jaw joints and muscles||Trauma, "wear & tear"||"TMJ syndrome"|
Headache types in bold are the common benign dysfunctional headaches. These are *idiopathic - ie no one really knows what causes them, but a complex interplay of hereditary, situational and stress factors seems to be involved in most people. Headache types shown in italics are the post-traumatic or toxic headaches that are the major focus of this review.
Headache "entities" enclosed in "quotation marks" are controversial, with dispute about their frequency, their cause, and sometimes their existence (see text).
Migraine, though usually a benign dysfunctional entity, may be aggravated or precipitated by trauma to the head and perhaps the neck.
These are discussed first because they are so common that there may be difficulty sorting them out from occupationally related headaches.
Why are they termed "benign dysfunctional" headaches? "Benign" speaks to the fact that the great majority of these headaches are nuisances rather than disabilities; they hardly ever produce long term inability to function; and they are never fatal. "Dysfunctional" means that the headaches are caused by intermittent malfunctioning of structurally normal tissues (such as, for example, the blood vessels of the head in migraine), and not by disease.
"Prevalence" denotes the number of people in a population who have a condition at any designated point in time. General population surveys have shown the prevalence of tension-type headaches in Canada to be 37% of females and 21% of males; in the U.S.A it is 42% of females and 36% of males, and in the U.K it is 35% of females and 29% of males. The differences reflect different techniques of data gathering and are inconsequential. The important thing is that these headaches are very common. Similarly, the prevalence of migraine in Canada is 23% of females and 9% of males; and in the U.S.A is 19% of females and 8% of males.
Tension headaches were given that name because at one time it was widely believed that they were caused by increased tension (contraction) of the muscles of the scalp and neck, which in turn was produced by increased emotional tension. An equivalent term was "muscle contraction headaches". The concept has fallen into disfavor because recordings of scalp and neck muscle activity in people with these headaches have not always shown increased muscle contraction. Few experienced clinicians would dispute that emotional tension (worry, anxiety, depression) plays a major role in producing these headaches, and the current hypothesis is that the head pain receiving centre of the brain (the nucleus caudalis trigeminalis) has had its sensitivity "turned up high" by increased activity of those higher centers of the brain which mediate stress, so that ordinarily innocuous stimuli are perceived as uncomfortable or painful. To accommodate the controversy, the International Headache Society coined the noncommittal term "tension-type headaches".
Tension-type headaches are dull, low grade aches which involve both sides of the head and may spread down into the neck. They may be mostly in the front, or mostly in the back of the head, or may invest the whole scalp, like a tight cap. The headaches are worse with anxiety but not usually with activity; indeed, many people with tension-type headaches will take a walk or do some other activity to divert themselves. Over-the-counter pain killers such as aspirin, Tylenol®, etc, usually bring some relief. Unlike migraine, there are no accompaniments to the headache such as nausea, vomiting, visual disturbance, or dizziness. The headaches typically last a half-hour to a day or two, and while most people have them only occasionally, a few may have them every day or almost every day; these people (whether as cause or effect) usually have significant psychological disturbances, such as depression.
Tension-type headaches are pretty nondescript. Having the 'flu, or an adverse reaction to a medication, or a brain tumor, can all produce a headache with similar features. Therefore, while often the entire picture (age, patient's circumstances and behavior, the general medical history, and the findings of a careful physical examination) makes this diagnosis evident, occasionally some special laboratory or neuroimaging tests (for example, CT scan) will be necessary before the prudent physician feels confident in diagnosing tension-type headaches.
Migraine, in contrast, exhibits a very specific pattern. The International Headache Society has formulated, validated and published clinical diagnostic criteria for migraine which are now the gold standard. These criteria stipulate that migraine is a recurrent headache, lasting a few hours to a few days, which has at least two of the following four features:
and which has at least one of the following two accompaniments:
and occurs in a patient who has nothing on history or examination to suggest another cause for the headaches.
If a headache fulfills these criteria, then it is migraine, and special tests are unnecessary for diagnosis (though they are frequently done for reassurance).
About one migraine patient in seven has an aura with some or all headaches, This aura, typically, is a visual disturbance that precedes the headache, lasts 20 to 30 minutes, and then clears as the headache appears. Sometimes there may be, as part of the aura, numbness or tingling of one side of the face and of the limbs on one side of the body; very rarely there may be weakness of the limbs. Many patients (and a few uninformed physicians) think that if there isn't an aura, then the headache can't be migraine; this is incorrect.
Migraine is a genetic disorder. More often than not, there is a history of migraine in a "first order relative" (parent, sibling, child). The headaches arise from episodic dilatation of the blood vessels of the head, both in the scalp and on the surface of the brain. The brain is believed to be the major driver of these vessel changes. Some triggers of migraine such as emotional stress, fatigue, exposure to certain frequencies of light, and likely the hormonal changes of the menstrual cycle, appear to work through the brain. Other migraine triggers, such as exposure to some substances in foods or in the environment, likely work through a blood-borne effect on the cranial blood vessels.
Migraine is most frequently treated with analgesics (pain killers), which is unfortunate for two reasons. First, these often aren't very effective and so the overuse of analgesics (particularly analgesics containing caffeine and/or codeine) resulting from vain attempts to get relief with them can itself produce chronic "rebound" headaches. Second, there are specific medications (the triptans) available which are much more effective in terminating the acute attack of migraine, and other medications are available for reducing the frequency of migraine attacks (migraine prophylactics). The expense of the triptans prevents many from using them, and the education of physicians regarding the wider use of migraine prophylaxis is a work in progress.
Many people complain to their physicians that things in their workplaces trigger, intensify, or generally aggravate their pre-existent headaches. Women are more likely to make this observation because, as noted above, they are more likely than men to have these headaches in the first place.
Emotional stress in the workplace can worsen both migraine and tension-type headaches, making them more frequent and sometimes more intense. Ergonomic factors, such as seating, desk height, cradling a telephone, etc can produce muscular stresses and strains that, in an individual subject to tension-type headaches, may trigger them. Some migraine patients feel that hours spent in front of a video display terminal precipitate and aggravate their attacks. Some migraine patients complain bitterly that the after-shave or perfume worn by their immediate co-workers triggers attacks. Some migraine sufferers implicate fumes, smoke, or just "poor ventilation" in the workplace. There is some scientific basis for all of these attributions.
Once triggered by an environmental factor, the migraine or tension-type headache will run its usual course, lasting anywhere from ½ hour (in the case of a tension-type headache) or a few hours (in the case of a migraine) to a few days, just like those not triggered by the environment. Identification and removal of the environmental trigger should result in the cessation of occurrence of the headaches. If the headaches do not stop occurring in the workplace once those factors blamed by the headache sufferer have been adequately addressed, then it becomes overwhelmingly probable that the headache sufferer was wrong, and that those factors never did play a part in causing the headaches.
The headaches following trauma, in contrast, tend to be much more refractory, and are a frequent source of disability and compensation claims. Head injury itself is remarkably common, being reported in about two million people in the USA every year (about 1% of the population). Forty-five percent of these injuries are due to motor vehicle accidents, thirty percent to falls, twenty percent to occupational and recreational accidents, and the remainder to miscellaneous causes including violence. Eighty percent of these head injuries are deemed mild, ten percent moderate, and ten percent severe, using as an index of severity the conventional criterion of duration of post-traumatic amnesia (the length of time after the injury for which the person has no memory). The incidence (the number of people in a population who develop a condition within a given time span) of post-traumatic headaches is highly variable, depending on the make-up of the population studied, and ranges from 30 to 70%. Older people are more likely to develop post-traumatic headaches, as are people who have had previous benign dysfunctional headaches such as migraine or tension-type headaches, and women. There is a paradoxical and controversial (see page 10) inverse relationship between the severity of the head injury and the likelihood of developing post-traumatic headaches. Some studies have shown that in societies (for example, a former Iron Curtain country) which do not have traditions of compensation for headaches or of private litigation, there is a much lower incidence of post-traumatic headaches than in neighboring NATO countries or in North America; these studies have provoked much emotionally-charged debate (see page 8 for a discussion of the controversy about physical versus psychological factors).
Injury to the neck, especially the so-called "whiplash" injury in which, as a result usually of a rear end collision in a motor vehicle, the head suddenly is propelled backward and forward, has been implicated as a cause of headache. Both head injury and whiplash-type neck injuries may be followed not only by headache, but by other symptoms including dizziness, imbalance, vertigo (a form of spinning dizziness, often precipitated by changes in posture), blurred vision, ringing in the ears, sensitivity to noise and bright light, fatigue, difficulty with concentration and memory, sexual dysfunction and personality changes such as irritability and depression. This concatenation of symptoms is called the "post-traumatic syndrome" generically, the "post-concussion syndrome" when it follows head injury, and the "whiplash syndrome" when it follows a neck injury.
These are the kinds of headaches that have been described following head or neck injury:
Much of the controversy over post-traumatic symptoms has to do with the common tension-type and the so-called cervicogenic headaches. In these situations, despite the individual's bitter complaints of nonspecific chronic headaches and of multiple other symptoms, there is usually no abnormality on physical examination or on neuroimaging (X-rays, CT scans, MRI, etc). Financial compensation is usually an issue. Controversy arises because there are no objective findings to corroborate these people's complaints or to substantiate their claims. As a result of this situation, two diametrically opposed positions on the genesis of post-traumatic headaches have emerged, and can be described as follows:
These are polar positions, presented as such for clarity. The dispute is not yet resolved, and is unlikely to be in the near future. Despite the very large number of people involved, the evidence which would settle the argument - autopsy confirmation or denial of microscopic damage in the brains of a series of people with persistent post-concussive symptoms and normal CT and MRI scans - is not at hand. For practical purposes, most physicians tend to approach their head-injured or "whiplash" patients on the basis that, in most cases, both psychological and physical factors may be involved and may necessitate treatment. Treatment is an empirical amalgam of physical and psychological measures. Note that in the two polar positions described above, the major difference in treatment is the vigor with which attempts are made to return the individual early to full activities. Note also that it is the tension-type headache and the often accompanying post-concussive/post-whiplash symptoms that are at the centre of the controversy; post-traumatic migraine, in contrast, has a generally agreed genesis and when diagnosed and treated appropriately, a generally good outcome.
There is an emerging consensus on how to diagnose post-traumatic headaches. The International Headache Society (IHS) has published diagnostic criteria for post-traumatic headaches. The type of headache is first established by how well it confirms to the IHS criteria for tension-type headache, migraine, etc. The issue of how likely that headache is to be causally related to head trauma is then assessed by the post-traumatic criteria, which are paraphrased as follows:
1. Headache follows significant head trauma , the significance being demonstrated by at least one of:
2. Headache begins within 14 days of trauma
3. If the headache disappears within 8 weeks following the trauma, it is termed "acute"'; if it does not, it is termed "chronic".
A headache that begins more than 14 days after the trauma is deemed unrelated to the trauma. A head trauma that does not meet the criteria for significance ("significant" does not necessarily equate with "severe", but rather with "not trivial") may still be followed by headache and other symptoms, but the causal relationship is then less definite.
The prognosis of post-traumatic headaches has been studied extensively, but the results of these studies have not been uniform because of:
Despite the shortcomings of the studies, a few factors have gained wide acceptance as being useful in predicting the outcome of post-traumatic headaches and other symptoms:
Other features are now widely regarded as not affecting prognosis:
Some prognostic features, even though extensively studied, remain controversial:
These headaches occur with use of, or exposure to, chemicals in the workplace or other environment. It is believed that most of the substances that produce headache do so by causing the pain-sensitive blood vessels of the head to dilate. A few substances (for example, the insecticides chlordecone [Kepone] and benzene hexachloride [Lindane]) may cause swelling ("edema") of the brain, which causes headache by increasing the pressure on the brain. Toxic headaches are diffuse, often throbbing, worse with activity, and of variable severity. It is believed, but not proven, that people who already have benign dysfunctional headaches such as migraine are more sensitive to some of these substances and are therefore more likely to develop headaches on exposure.
Carbon monoxide is probably the most common cause of environmental headaches (malfunctioning heating systems, poorly-ventilated auto shops), but there are many other substances which have been identified as causing headaches. The following list is far from exhaustive:
The headaches clear once the individual is removed from the environment, and typically this clearing occurs quickly, usually within a day or two, as the dilated cranial blood vessels return to normal. It may be delayed for weeks, however, if the toxic substance has accumulated in the body (eg lead) or if the headache is mediated by brain edema, which may take some time to subside.
Certain factors assist in the diagnosis of these toxic headaches:
A vexatious problem is the case of the individual who claims headaches to be occurring on the basis of sensitivity or allergy to a non-toxic substance within the environment, or hypersensitivity to substances present in acceptable levels (for example, dust). There is no question that some forms of allergy like serum sickness, anaphylaxis, urticaria, and rhinitis complicated by sinusitis may cause headaches among other prominent symptoms (such as wheezing, hives, collapse of blood pressure, etc). What is extremely controversial is whether or not hypersensitivity or allergy can cause headaches alone. In cases such as this, resolution may be aided by the finding in blood cells, plasma, cerebrospinal fluid and/or urine of chemical or cellular evidence of an acute allergic reaction during a headache; such evidence can be provided by an immunologist or allergist. A positive skin test is not enough to link the probable presence of an allergy (which is what the skin test signifies) with the headache; both allergy and headaches are extremely common as independent entities in the general population.
The above seven papers are a sampling of views about post-traumatic symptoms and how societal factors such as expectations and compensation influence, or do not influence, their development and persistence. The editorial by Deyo (ref. 8) is a current, brief, and well-balanced overview.