Research Review By Dr. Robert Rodine ©

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Date Posted:

January 2011

Study Title:

Stress and tension-type headache mechanisms

Authors:

Cathcart et al.

Author's Affiliations:

Centre for Applied Psychological Research, School of Psychology, University of South Australia

Publication Information:

Cephalalgia 2010; 30(10): 1250-1267.

Background Information:

As we know, headaches are classified, according the IHS, into either primary or secondary headaches. A primary headache is one that is not attributable to a secondary disease process, therefore is manifesting directly, and is classified according to its symptoms. These include tension-type headaches and migraine, and more rarely, cluster headache and trigeminal neuralgia. A secondary headache on the other hand, is a form of headache disorder due to another etiology, a secondary disease process elsewhere in the head and neck. These disorders are classified according to the etiology rather than the symptoms.

Tension-type headache is the most common type of primary headache, representing ~80% of all headache diagnoses. (Now, the accuracy of those diagnoses can obviously be called into question given the controversy surrounding tension-type headache versus cervicogenic headache. But that is a different review all together.)

Stress, from work, daily-life, relationships etc., has been found to be the most common headache trigger (1,2). As a result, previous hypotheses have estimated the effect which stress would have on muscle tension, therefore causing or aggravating headaches in sufferers (3). Unfortunately, this hypothesis has not been strongly supported.

The purpose of this review is to explore the possibility that stress may contribute to Tension-Type Headache (TTH) through a sensitizing effect of the pain processing pathway. Therefore, the cited paper reviews three particular topic areas:
  1. specific pain mechanics of TTH;
  2. the relationship between stress, pain and head pain mechanisms; and
  3. the relationship between stress and pain processing in TTH.

Pertinent Results:

Mechanisms of TTH

Muscle Contraction:
  • Muscle contraction leading to ischemia or the development of trigger points was previously thought to be the cause of TTH. However, no evidence has been identified showing an increase in muscle tension, as surface EMG studies have found no, or only a minimal, increase in pericranial muscle tension in TTH sufferers.
  • EMG levels have not correlated with stress levels or stress-induced headaches in TTH sufferers.
  • For example, one cross-over designed study evaluated TTH subjects who were either exposed to a placebo (undefined) versus jaw clenching. The results found no difference between groups with respect to the number of subjects who developed headaches (4).
  • A further study compared TTH sufferers to healthy controls and examined the effect of static trapezius contraction on the development of headache symptoms. It was found that TTH sufferers developed significantly more headaches as a result of the experiment (5). Therefore, the authors concluded that the act of muscle contraction itself was not responsible for the results and that it was only one part of the mechanism (if muscle contraction were the primary mechanism, all patients would have shown equal incidence of headache).
Myofascial Tenderness:
  • Increased muscle tenderness is thought to be related to TTH given that: it has been linked to headache history and severity, it is increased during a headache episode and it precedes headache episodes subsequent to voluntary muscle contraction.
  • This leads to the hypothesis that this represents a peripheral disorder causing sensitization of the myofascia OR a central disorder causing sensitization at the spinal/trigeminal dorsal horns.
  • However, muscle biopsy in ETTH sufferers has proven unremarkable, and central processing to mechanical, thermal or electrical stimulation has equally been proven normal. This is untrue for CTTH however.
  • Central mechanisms appear to be abnormal in CTTH sufferers given increased responses to pain stimulation.
  • Also, as muscle tenderness increases in CTTH sufferers, pain thresholds decrease, indicating a relationship with central sensitization.
  • This being said, other studies have failed to show a correlation between muscle tenderness and TTH, therefore another factor must be considered, such as endogenous pain regulatory mechanisms.
Central Sensitization

Spinal/Trigeminal Sensitization
  • Central nucluei in the trigeminal nucleus caudalis receive convergent input from the pericranial muscular, vascular, trigeminal and cervical nerves of the neck and shoulders, in addition to the head itself. As a result, a neural interplay exists between these structures and supra-spinal structures. (for reference, this link is the proposed mechanism behind the vascular-supra-spinal-myogenic {VSM} model of migraine, as well as TTH).
  • Abnormal trigeminal and trigemino-cervical reflexes in CTTH sufferers suggest a link at this level. More importantly, increased sensitivity is noted generally and not just within muscular structures.
Supra-spinal Sensitization
  • This specifically refers to sensitization of the third order neurons, in the thalamic or cortical areas.
  • Recent imaging studies have identified cortical abnormalities in CTTH sufferers in the areas of the pons, anterior cingulated cortex, insular cortex, temporal lobe, orbito-frontal cortex and hippocampus. These areas all have functions pertaining to pain processing and demonstrate consistent decreased tissue mass in CTTH sufferers. It is still unclear however if the atrophy is the primary cause or a secondary response.
  • Additionally, atrophy could be the result of prolonged activation from lower structures which are conveying noxious stimuli.
Temporal Summation
  • Temporal summation, or ‘wind-up,’ is the process whereby noxious stimulation delivered consistently generates a cumulative activation of neurons that does not return to baseline.
  • This phenomenon is suggested to be the reason by which prolonged myofascial input results in central sensitization in TTH sufferers.
  • Studies examining this phenomenon specifically in TTH sufferers have been conflicting however, as results have not shown significant trends or demonstrated no difference between TTH subjects and healthy controls.
Pain Modulation
  • Another proposed central mechanism involved in TTH pain is a deficiency of pain modulation and inhibitory mechanism rather than, or in addition to, central sensitization (see Related Reviews below)
  • One study examined the effect of pressure pain thresholds at the finger following an experimentally sustained muscle contraction in the jaw. In those subjects who did not experience a headache following the contraction, their pressure pain thresholds were increased. In other words, they exhibited an anti-nociceptive response. Alternatively, those subjects who did experience a headache after muscle contraction demonstrated no change in pressure pain thresholds. This is thought to indicate an impaired inhibitory system.
Psychological Pain Processing
  • Lastly, pain response could be due to psychological changes, such as anticipation, hypervigilance and increased attention, increased reporting or effects on the meaning of pain.
  • This is relevant to TTH as sufferers have been found to have poorer coping mechanisms, poor memory recall of previous episodes and increased arousal. Also, anxiety, depression and anger have been shown to be higher in TTH sufferers.
Stress and Pain

Based on the shared responses with the neural, endocrine and autonomic systems, as well as behavioral mechanisms, stress and pain are closely related.

While nociceptive stimulation activates the stress system, stress results in a release of epinephrine which can aggravate sensitized nociceptors. This is one simple connection. The link becomes even more complex when examining the midbrain and the inter-relationships between the hypothalamic pituitary adrenocortical and sympathetic adrenomedullary axes, the periaquaductal grey, the rostroventral medulla, etc.

As a result of this complex system, stress can have both an inhibitory and an excitatory effect on pain processing.

Inhibitory Effects of Stress:
  • Based on observations of wounded soldiers in battle, stress has been thought to play an inhibitory effect on pain processing, thus enabling us to either fight or flee in spite of pain/injury. However, this is only true in situations of acute psychological stress whereby our attention is focused on the stressor, rather than on the pain.
  • This type of response is an important survival instinct.
Excitatory Effects of Stress
  • Pain processing can be facilitated by stress in situations of sustained arousal, negative mood states, anxiety, chronic or daily stress or even from poor coping strategies.
  • These links are also thought to be a survival instinct, whereby our response to a stressor helps us avoid a similar situation in the future.
Stress as the Cause of Pain
It has been suggested that, given the complex link between pain and stress pathways, stress may cause pain in the absence of an incoming noxious stimuli. This is likely due to the limbic system potentially binding the two systems together.

Stress and Pain Processing in TTH
  • TTH sufferers have been found to have higher levels of stress than healthy controls (6).
  • TTH sufferers have been found to have higher levels of cold pressor pain than healthy controls (6).
  • This findings are a bit controversial, as other results have demonstrated that sufferers were found to only have higher levels of stress than healthy controls, without a change cold pressor pain levels (7).
  • Catastrophizing has also been found to a higher degree in sufferers versus healthy controls (8).
  • Linkage between muscle tenderness and anxiety levels in TTH sufferers has been difficult to determine, as study results disagree widely.
  • Stress has been linked to pain sensitivity as an effect. Pain experienced on exertion has been found to be increased in TTH sufferers following an hour long task which induced stress (9).
  • When muscle tenderness and pain thresholds were tested in a group of depressed TTH sufferers, muscle tenderness was found to increase following an hour long stressful task. Additionally, depressed TTH sufferers were more likely to experience a headache following the task (9).
  • A series of articles completed by Cathcart et al. have found that stress induces an increased pain sensitivity in TTH sufferers versus healthy controls.

Clinical Application & Conclusions:

The authors’ primary objective within this manuscript was to suggest that stress may contribute to, or aggravate the abnormal pain processing within TTH sufferers.

This information is helpful in clinical practice, taken with limitations into consideration, as it allows clinicians to generate a more accurate and reasonable prognosis.

When stress is apparent in a TTH patient, we may assume that pain processing, interpretation and coping behaviors may be different. This can create a negative prognosis for the patient. Therefore, they may experience their symptoms for a longer time frame to resolution than a non-stressed individual, or they may not respond in at all to a particular intervention.

Next steps in research could be to examine the same group of TTH sufferers to determine:
  1. How to effectively modify daily stress in their lives;
  2. how to modify their coping behaviors; and
  3. if these modifications offer a more favorable prognosis for the patient and their headache patterns.

Study Methods:

This review follows that of a narrative format, with no information regarding the literature search strategy or results provided.

The authors made all efforts available however to limit studies to those examining TTH specifically. When possible, TTH was sub-divided into chronic TTH (CTTH) or episodic TTH (ETTH). Also ETTH was also subdivided into frequent and infrequent ETTH.

Study Strengths / Weaknesses:

The authors of the study offer the following limitations to their own work:
  • To date, the evidence base which examines the direct effect of stress on experimental pain is minimal
  • The evidence base examining the importance of stress as an aggravator is equally minimal.
  • Future research is also needed to examine the specifics aspects of pain which are affected by stress.
  • Greater understanding is needed to examine how stress affects pain processing.
The major limitation of this work is its narrative structure. The study’s search results and presentation are in no way systematic, and therefore biased.

More importantly, while the authors outline a reasonable and linear pathway to their hypothesis, the information itself becomes confusing.

Throughout many sections, evidence is presented supporting their hypothesis. Then evidence is presented refuting the previous findings. After this pattern is repeated many times, it becomes confusing as a reader. You are unsure of how they are eventually going to support their theory. This is made clear in the end with a short paragraph describing several referenced works written by the primary author that do in fact support the theory. Prior to this, most evidence is presented which only indirectly supports their hypothesis.

This aside, their theoretical presentation is sound and offers clinical consideration.

Additional References:

  1. Martin et al. Towards a functional model of chronic headaches: investigation of antecedents and consequences. Headache 1993; 33: 461-470.
  2. Nash et al. Understanding psychological stress, its biological processes, and impact on primary headache. Headache 2006; 46(9): 1377-1386.
  3. Ah Hoc. Classification of headache. JAMA 1962179: 717-718.
  4. Neufeld et al. Dynamic assessment of abnormalities in central pain transmission and modulation in tension-type headache sufferers. Headache 2000;40(2):142-151.
  5. Christensen et al. Experimental induction of muscle tenderness and headache in tension-type headache patients. Cephalalgia 2005; 25(11): 1061-1067.
  6. Hatch et al. Electromyographic and affective responses of episodic tension type headache patients and headache free controls during stressful task performances. J Behav Med 1992; 15(1): 89-112.
  7. Cathcart et al. Effect of mental stress on cold pain in chronic tension type headache sufferers. J Headache Pain 2009; 10(5): 367-373.
  8. Ukestad et al. Pain perception and coping in female tension headache sufferers and headache-free controls. Health Psychology 1996; 15(1): 65-68.
  9. Leistad et al. Stress-induced pain and muscle activity in patients with migraine and tension-type headache. Cephalalgia 2006; 26(1):64-73.
  10. Janke et al. Depression increases onset of tension-type headache following laboratory stress. Pain 2004; 111:230-238.