Tension-type headache
Tension-type headache (TTH) is the most common type of primary headache. It is not considered to be a disease, but a group of clinical syndromes caused by various reasons, including myoconstriction headache in 1962, Tension Headache, common headache, functional headache, and psychogenic headache. It was not until 1988 when the classification committee of the International Headache Society (IHS) proposed the new term “Tension-Type Headache (TTH)” that the nomenclature was unified and then subdivided into various subtypes, each of which was given clear diagnostic criteria. In January 2004, the IHS Classification Committee continued to use Tension-Type Headache (TTH) in the second edition of the new headache classification. Studies have shown that the prevalence of tension-type headache varies from 30% to 70% over a person’s lifetime. People with episodic headaches that are relieved by aspirin or paracetamol, or episodic neck and scalp muscle tension that can be relieved by massage, rarely consult a physician. In contrast, most patients with psychogenic headache who seek medical attention often have daily or uninterrupted episodes of headache that are not relieved by simple analgesics or even narcotics (unlike the pain of intracranial occupants), for months or years. These patients are difficult to describe, and the diffuse aching or pressure sensation pain may be distributed in the occipitotemporal or frontal regions, but is always bilateral. The unilateral throbbing character of migraine is uncommon and is not usually accompanied by vegetative symptoms such as nausea, vomiting, photophobia, and phonophobia. The disease affects the work, study and rest of patients, which brings great psychological burden to patients and families, and also brings great socio-economic impact.
I. Epidemiology
In recent years, foreign scholars have investigated the epidemiology of TTH, including gender, age, susceptibility factors, peak incidence, education level, area of residence, and one-year prevalence. Population-based research studies in Western Europe and North America have shown that the annual prevalence of TTH ranges from 30% to 80%, with differences that may be due to differences in research methods and definitions.Rasmussen noted that the lifetime incidence of headache in patients with TTH is 78%, with a ratio of 4:5 for both sexes, and that the prevalence of TTH decreases with age; the age of headache onset is mainly in the 20s. Previous epidemiological surveys have shown that 24% of patients with TTH have headaches for 8 to 14 days in a year, and 41% for more than 14 days. The prevalence of chronic tension-type headache (CTTH), i.e., headache for ≥180 days in a year, is 3%. the most common precipitating factors for TTH are stress and nervousness, and alcohol consumption, smoking, and climate change are also common precipitating factors. The epidemiological survey by Gobel in Germany detailed that the lifetime incidence of episodic tension-type headache (ETTH) was 36%:34% for both sexes, which was close to 1:1; the incidence of CTTH was about 3% for both sexes, which was consistent with Rasmussen’s report. These results suggest that there is no difference in the incidence of TTH between the sexes. Gobel also found that the incidence of CTTH increased with age, with a 2% incidence in the 18-35 age group, 3% in the 36-55 age group, and 4% in the 56+ age group. The incidence of E T T H did not vary with age. there was no significant correlation between TTH and factors such as level of education and residence in town or country, but the female menstrual cycle was a susceptibility factor.
II. Etiology and pathogenesis
Common etiologies of ETTH include contraction of the posterior occipital and shoulder muscles due to poor head, neck, and shoulder posture, lack of rest and sleep deprivation, temporomandibular joint dysfunction, anxiety and depression, overdose and abuse of pain medications, neuroticism, psychosomatic tension resulting from various stressors, including marital problems, occupational problems, interpersonal tension, cultural and religious problems, low economic income, legal disputes, physical illness The common causes of CTTH are overdose or abuse of pain medication, and headache can disappear or be converted to ETTH after the medication is stopped in such patients. Anxiety and stress are common precipitating factors for ETTH.
The pathogenesis of tension-type headache is not well understood, and there are various theories, such as psychological theory, muscle contraction mechanism, central mechanism, myofascial mechanism and genetic factors. The common triggers are contraction of the posterior occipital and shoulder muscles due to poor head, neck and shoulder posture, lack of rest and sleep, temporomandibular joint dysfunction, anxiety and depression, pain medication overdose and abuse, and psychological stress. Recent studies have shown that the development of tension-type headache has a neurobiological basis, especially in the more severe subtypes. For example, local accumulation of pain-causing substances such as 5-hydroxytryptamine, lactic acid and bradykinin; intracellular and extracellular potassium ion transport disorders; and blood circulation disorders in muscles and myofascia can lead to tension-type headache.
1.Theories of psychological mechanism: The theories on psychosomatic processes are divided into two parts: 1) emphasizing the role of emotional processes; 2) focusing on cognitive processes. These views can explain many symptoms of TTH, including somatic symptoms and psychological disorders. The emotional theory doctrine suggests that pain due to psychogenicity can act as a solution to non-conscious conflicts in the body. Patients with pain have a need to satisfy the aggressive impulses of others, and in lieu of an external response this aggression is directed at themselves rather than others. Although a few researchers have found that TTH patients are consciously disturbed by hostile feelings and anxiety, this in vivo nonconscious conflict has not been observed in experiments to date. The cognitive theory emphasizes the role of attentional processes in pain. This theory suggests that the body’s endogenous sensations compete with acquired external environmental sensations, and that somatic sensations may have higher perceptibility when external environmental stimuli are reduced (e.g., deprived of all stimuli) or when mental activity is increased (e.g., stressful). When a person assembles these perceptions through cognitive procedures, the symptoms of the organism can be explained by these perceptions. As with the emotion theory, it has not been tested so far in TTH patients.
2. Muscle contraction mechanism Continuous contraction of the pericranial muscles is a classical theory in the mechanism of TTH occurrence. The basic idea is that headache-promoting factors cause the pericranial muscles to be in a continuous state of contraction, compressing the small intra-muscular arteries and producing muscle ischemia and tenderness and pressure pain. The contraction of the skeletal muscles is emphasized as the basic cause of headache. muscle tenderness and pressure pain in TTH patients is directly confirmed by many studies. tenderness in the pericranial muscles is significantly higher in TTH patients, and muscle stiffness decreases after clinical symptoms improve.
3. central mechanisms There has been recent emphasis on the prerequisite role of central mechanisms in the pathogenesis of TTH, with muscle factors not being the primary cause but the consequence. It is speculated that there may be a decrease in inhibitory interneuron activity in the brainstem and limbic system, and a decrease in inhibitory interneuron activity in CTTH patients.
4. myofascial mechanisms Unlike central mechanisms, muscle factors are thought to play an important role in the initiation of headache; further development and transformation into a chronic pain state. Random muscle contraction due to mechanical or psychological tension causes activation of myofascial mechanoreceptors and their afferent fibers; this increase in pericranial muscle afferents can cause sensory and functional reorganization of second-level sensory neurons in the posterior horn of the gray matter of the spinal cord. Under normal conditions, increased peripheral sensory injury afferents are resisted by increased activity of the anti-sensory injury system and do not cause headache. However, under certain circumstances, this self-stabilizing mechanism is lost, producing abnormal sensory effects; together with damage to the central anti-sensory system, a TTH attack can be produced.
5.Nitric oxide (NO) factor Research shows that NO plays an important role in the pathophysiology of primary headache, especially migraine and CTTH. nitric oxide synthase inhibitors can reduce the degree of TTH and muscle hardness, while nitroglycerin, the donor of NO, is more likely to cause late-onset TTH.
6. Platelet factors During TTH attacks, the level of 5-HT in platelets decreases, while the level of plasma 5-HT increases, suggesting that this amine is involved in the pathophysiological process of TTH, but in a way that may be different from that of migraine. In addition, intraplatelet Met-enkephalin decreases during headache and increases in plasma, presumably because Met-enkephalin has an anti-endothelial damage effect on 5-HT and is released together with 5-HT during headache attacks. An increase in platelet γ-aminobutyric acid (GABA) levels during TTH attacks has also been reported, which may be similar to migraine, where neurons are in a hyperexcitable state during TTH attacks and GABA is an important inhibitory neurotransmitter in the central nervous system. GABA is elevated in platelets during headache attacks to counteract the hyperexcitability of central neurons. In conclusion, platelet abnormalities are present in TTH patients, but their role in the pathogenesis of TTH is unclear.
7. Immune mechanisms Some studies have shown that B lymphocyte expression is enhanced in CTTH patients, but plasma immunoglobulin (Ig) is not elevated. However, severe psychological depression may have an impact on the immune system of TTH patients, so immune abnormalities may not be the cause.
8. Vascular factors Some patients with TTH have increased cerebral blood flow during attacks, which can produce pulsatile headache, similar to migraine without aura; and 5-HT1D receptor agonists are also effective in patients with TTH. It is suggested that there may be vascular mechanism involved in TTH.
9. Others: Genetic factors may also be involved in the pathophysiological process of TTH and increase its susceptibility. TTH is often associated with anxiety, depression, anger, and hostility, and antidepressant drugs are effective in its treatment, suggesting that psychiatric factors are related to TTH attacks. However, these mood changes are currently thought to be the result of chronic headache. It is newly believed that CTTH may be mostly or solely determined by genetic factors.
III. Clinical manifestations
The disease tends to start in the early 20s and is more common in women. The pain is located in the bilateral occipital neck, frontotemporal region or the whole head, manifesting as distension, head pressure or tightness, headache is episodic or persistent, and the duration of the disease varies from several days to several years. There may be tenderness or pressure pain in the muscles at the site of pain, and sometimes hair pulling pain. The head, neck and back muscles may feel stiff. Most patients are accompanied by anxiety, depression, insomnia and other symptoms.
IV. Diagnosis
The disease should mostly be considered in adults with prolonged tightness and/or distending pain in bilateral temporal, occipitotemporal, posterior occipital or around the head that occurs during daily activities. It is more likely if bilateral temporal, suboccipital and other muscular pressures are painful.
International classification of tension-type headache (TTH)
The first edition of the International Classification of Headache: In 1988, the IHS Classification Committee divided TTH into 3 categories: (1) Episodic Tension-Type Headache (ETTH), which includes 2 types: (1) episodic tension-type headache with pericranial muscle contraction; (2) episodic tension-type headache without pericranial muscle contraction. (2) Chronic Tension-Type Headache (CTTH), which also includes two types: (1) chronic tension-type headache with pericranial muscle contraction; and (2) chronic tension-type headache without pericranial muscle contraction. (3) Tension-type headache that does not meet the above diagnostic criteria.
The second edition of the International Classification of Headache: In January 2004, the IHS Classification Committee released the second edition of the International Classification of Headache, and the new classification divided TTH into four categories. The new classification mainly distinguishes ETTH into sporadic ETTH and frequent ETTH according to the duration and number of attacks. this time, TTH is classified into the following types.
(1) Infrequent Episodic Tension-Type Headache (IETTH), which includes two types: (1) sporadic episodic tension-type headache with pericranial pressure pain; (2) sporadic episodic tension-type headache without pericranial pressure pain.
(2) Frequent Episodic Tension-Type Headache (FETTH), which also includes two types: (1) frequent episodic tension-type headache with pericranial pressure; (2) frequent episodic tension-type headache without pericranial pressure.
(3) Chronic Tension-Type Headache (CTTH), which also includes the following two types: (1) chronic tension-type headache with pericranial pressure pain; (2) chronic tension-type headache without pericranial pressure pain.
(4) Possible tension-type headache, including: (1) possible infrequent-onset tension-type headache; (2) possible frequent-onset tension-type headache; (3) possible chronic tension-type headache.
V. Differential diagnosis
The diagnosis of this disease must exclude other causes of various headaches and diseases in the facial pain syndrome. Among them, it should be distinguished from various major organic diseases such as nasopharyngeal carcinoma, cranial tumor, glaucoma, intraorbital tumor, mastoiditis, pterionitis, pituitary tumor, hypertension, temporomandibular joint disease, parotid gland disease, etc.
1.Cervicogenic headache: This disease is mostly seen in middle-aged and elderly people, often cervical-occipital episodic headache, easily triggered by head and neck rotation or forward and backward flexion, may be accompanied by vertigo, shoulder and arm numbness or pain, limited neck movement, cervical paravertebral pressure pain, cervical frontal and lateral, oblique film can see osteophytes, cervical intervertebral foraminal stenosis, etc.. MR examination of cervical spine can find cervical disc prolapse.
2.Posterior cranial fossa tumor: This disease is caused by tumor compression or edema pulling the cerebellar curtain, which can lead to pain in the posterior occipital region, starting with intermittent dull pain, and later developing into persistent severe pain, often accompanied by the manifestation of increased intracranial pressure such as jet vomiting, optic papillary edema, etc. The diagnosis can be confirmed by cranial CT or MR.
Occipital neuralgia: the pain can be paroxysmal or continuous pain in the occipital and upper neck on one or both sides, sometimes it can be extended to the posterior mastoid process, the pain is more superficial, intense like electric shock or burning, often accompanied by neck and shoulder pain or numbness and pain in one limb when hyperextension and hyperflexion, and there are pressure points at the outlet of occipital nerve.
VI. Treatment
Since tension-type headache is the result of the combined effect of multiple factors, its treatment should emphasize the comprehensive treatment according to different individual characteristics.
1.Psycho-behavioral therapy: It is necessary to explain the nature of the disease to the patients and their family members, to provide timely psychological guidance to the patients, to make them release unnecessary worries, to maintain optimism and optimistic spirit, to have regular daily life, and to participate in cultural and sports activities frequently. This is a prerequisite for successful treatment. It also includes withdrawal of dependence on drugs, consultation with a psychiatrist, and cognitive-behavioral therapy. Psychotherapy is appropriate for children and adolescents with TTH who are substance abusers or overdose, with comorbid psychiatric disorders. Commonly used methods include: EMG biofeedback training, which helps patients learn to control tension for 30 minutes a day; relaxation training methods, including progressive relaxation training (PRT) and natural training, which passively regulates the mind and body.
2 .Physical relaxation therapy: occipito-cervical, frontotemporal muscle massage, electrical excitation, thermal biofeedback and acupuncture treatment can achieve the purpose of relaxing the neck and shoulder muscles. Physiotherapy: including transcutaneous electrical nerve stimulation, massage, relaxation training, etc. Relaxation should master certain skills, firstly, in a light-proof environment, adopt a comfortable reclining posture and start training; then, sit in a place where the surrounding environment is not too quiet for training; finally, you must insist on practicing every day. Correct bad posture. In addition, home-based training procedures sometimes even exceed the effectiveness of clinical treatment. The following procedure is very helpful in relieving TTH: (1) sit in a chair with your back tight, hands on your knees, and feet on the floor; (2) lean your head against the wall; (3) lower your shoulders; (4) relax your jaw, leaving a gap between your upper and lower teeth; (5) close your eyes and breathe calmly and rhythmically; (6) feel your whole body relaxing from head to toe; (7) choose a cue word each time you inhale, such as “relax”; (8) after 30 seconds, open your eyes and end with a deep breath. The evaluation of hypnotherapy, biofeedback, meditation (maditation) and other relaxation techniques in the treatment of psychogenic headache has not been determined.
3. Anti-anxiety and depression drugs: Prozac 20mg/day or Zoloft 50mg/day can be used. These drugs inhibit the reuptake of 5-hydroxytryptamine in the central nervous system. In addition, tricyclic depressants such as amitriptyline 25mg/day twice a day and 25 mg at bedtime can reduce the number of attacks and shorten the duration of headache.
4.For patients with insomnia, use sedative drugs: such as Sulezade, clonidine, etc.
5.Pain relief drugs: NSAIDs such as acetaminophen, ibuprofen, naproxen, etc. can be used as pain relief drugs. In the treatment of chronic tension-type headache, Tizanidine (Tizanidine) can be used at a starting dose of 6 mg/day (divided into 3 doses), and the dose can be increased gradually up to 18 mg/day for 6 weeks according to the treatment response. Ibuprofen 200 mg/tablet, 1 tablet 3 times daily. Its extended-release tablet is fenpropathrin 300 mg/tablet twice daily. Anti-inflammatory pain 25mg, 1 tablet twice daily. Ketoprofen 50mg/tablet, 1 tablet 3 times a day and Naproxen 200mg 3 times a day, preferably with meals. In some patients, caffeine or anti-anxiety and tension medication can be added to enhance the pain relief effect.
6.Other:
For some patients with tension-type headache of migraine nature, the addition of β-blockers such as Jinan 20 mg/time, 3-4 times/day, or calcium antagonist treatment can enhance the efficacy of amitriptyline.
Patients with tension-type headache especially with significant pericranial muscle pressing pain are effective with myorelaxants. Oral muscle relaxants. Central muscle relaxants: (1) Mephentermine analog Chlormezanone (Fenarol) 200mg Tid; chlorzoxazone 200mg Tid; phenprobamate 200mg Tid; tolperisone 50mg Tid (2) GABA-like compounds; Baclofen 5mg Bid~Tid; Diazepam 2.5~5mg Bid~Tid; (3) Tizamidine 2~4mg Bid~Tid (3) Tizamidine (Songdele) 2～4mg Tid.
Direct-acting muscle relaxant Dantrolene (Dantrolene) 25mg/d, plus 25mg weekly 100mg Tid after 7 weeks.
The efficacy of muscle relaxants for the treatment of tension-type headache varies from report to report. Myona is useful for the treatment of tension-type headache 50mg/d twice/day. Myona has few adverse effects, with diarrhea, upright hypotension, dizziness, and rash in a very small number of patients, which can disappear after discontinuation of the drug. A few authors have also concluded that the efficacy is indeterminate.
In most patients with refractory chronic tension-type headache, intravenous dihydroergotamine (DHE) is effective.
7. Prophylactic drug therapy
As preventive therapy for tension-type headache, non-pharmacological treatment such as lifestyle modification, relaxation training and psychotherapy are more important than pharmacological treatment.
1.Antidepressants: tricyclic antidepressants such as amitriptyline and chlorpromazine can enhance their efficacy when used in combination with beta-blockers (insulin). Amitriptyline was used earlier for the treatment of patients with chronic tension-type headache with depression, and this drug is a norepinephrine and 5-HT reuptake inhibitor. The oral dose is started at 75 mg/d and increased to 150 mg/d in divided doses. Side effects include nausea, vomiting, fatigue, drowsiness, dizziness and insomnia. The efficacy of antidepressants in the treatment of tension-type headache is about 10-46% for amitriptyline, 32% for maprotiline, and 15% for doxepin. SSRI antidepressants: such as Bacitracin, sertraline, paroxetine, etc. These drugs are effective and have few side effects.
2, muscle relaxants: 50% to 60% of TTH patients, related to pericranial muscle disorders, the use of muscle relaxants can be alleviated. Commonly used muscle relaxants are: central muscle relaxants, such as chlorambucil, valium, tetonidine, cyclobenzaprine hydrochloride, etc. Peripheral muscarinic agents, such as dantrolene.
Brofort found through bulk literature review statistics that the use of chiropractic in the prophylactic treatment of chronic tension headache obtained short-term efficacy similar to that of amitriptyline.
VII. Prognosis
Frequent episodes of E T T H may evolve into CTTH after several years.The main factors affecting the prognosis of TTH are the following. ①Severity of TTH: Since TTH, migraine and drug-induced headache often coexist clinically. (ii) Combined migraine: It is currently believed that patients with TTH who have combined migraine have more severe attacks and more frequent attacks. (③) Drug overdose and abuse: The most common cause is overdose of combined painkillers, ergotamine or sumatriptan. Long-term abuse is the most common cause of TTH evolving from episodic to chronic and finally to chronic daily headache. Unless these pain medications are discontinued, the patient will be in worse clinical condition and will be resistant to all preventive treatments. ④Psychosocial stress: The severity and frequency of TTH headaches are related to the patient’s ability to deal with daily chores, and poor ability to deal with daily chores is associated with poor prognosis of headaches. ⑤ Sex hormones: Menstruation can promote migraine attacks as well as TTH attacks, so it seems that fluctuations in plasma sex hormone levels are related.
Studies with large samples have shown that the prognosis of FETTH and CTTH is good; FETTH is converted to IETTH or the headache is terminated by treatment, and the poor outcome of some CTTH patients is related to combined migraine, marital problems, and sleep problems. In conclusion, the prognosis of TTH also depends mainly on the recognition and diagnosis of TTH, early and specific treatment, and avoidance of inappropriate overdose.