Trigger Points

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Definition/Description[edit | edit source]

A Trigger Point (TrPt) is a hyperirritable spot, a palpable nodule in the taut bands of the skeletal muscles' fascia. Direct compression or muscle contraction can elicit jump sign, local tenderness, local twitch response and referred pain which usually responds with a pain pattern distant from the spot.[1] [2] [3] [4] [5]

Jump sign is the characteristic behavioural response to pressure on a TrPt. Individuals are frequently startled by the intense pain. They wince or cry out with a response seemingly out of proportion to the amount of pressure exerted by the examining fingers. They move involuntarily, jerking the shoulder, head, or some other part of the body not being palpated. A jump sign thus reflects the extreme tenderness of a TrPt. This sign has been considered pathognomonic for the presence of TrPts [4]

Local twitch response - defined as a transient visible or palpable contraction of the muscle and skin as the tense muscle fibers contract when pressure is applied. Coursed by needle penetration or by transverse snapping palpation. [2][3]

Referred pain, also called reflective pain, is pain perceived at a location other than the site of the painful stimulus. Pain is reproducible and does not follow dermatomes, myotomes, or nerve roots. [3][4] There is no specific joint swelling or neurological deficits[3].

Kinds of referred pain: 

  • peripheral: the TrPt is located outside the referred zone,
  • mostly central: the trigger point is located inside the referred zone but the hotspot lies elsewhere, 
  • local: TrPt lies in the hotspot of the referred pain.

(Radiating pain is slightly different from referred pain; for example, the pain related to a myocardial infarction could either be referred or radiating pain from the chest. Referred pain is when the pain is located away from or adjacent to the organ involved; for instance, when a person has pain only in their jaw or left arm, but not in the chest)[1][2][3][4][6]

Anatomy and Etiology[edit | edit source]

Trigger points develop in the myofascia, mainly in the center of a muscle belly where the motor endplate enters (primary or central TrPs)[7]. Those are palpable nodules within the tight muscle at the size of 2-10 mm and can demonstrate at different places in any skeletal muscles of the body. May be present even at babies and children.

Causes - Usually, TrPs happened due to:

  • aging,
  • an injury sustained by a fall, by stress or birth trauma.
  • a lack of exercise - commonly in sedentary persons between 27,5-55 years of which 45% are men[8],
  • a bad posture[9] - upper and lower crossed pattern, swayback posture, telephone posture, cross-legged sitting,
  • muscle overuse and respective micro trauma - weightlifting,
  • cronical stress condition - anxiety, depression, psychological stress trauma,
  • vitamins deficiencies - vitamin C, D, B; folic acid; iron;
  • sleep disturbance,
  • joint problems and hypermobility.

Recent literature introduced two differing hypotheses for the basic of TrPs: 1. dysfunctional muscle spindles; 2. dysfunctional extrafusal neuromuscular junctions. Electrophysiological investigations of TrPs reveals phenomena which indicate that the electrical activity of active loci arises from dysfunctional extrafusal motor endplates rather than from muscle spindles[10][11].

Classification of TrPs[edit | edit source]

TrPts can be divided in several groups [2][3][4][5]: 

Primary / Central AND Secondary / Satellite Trigger Points
  • Primary or Central TrPs are those that cause severe pain locally at the pressure with irradiation according to referred pain map. Usually are based around center of a muscle belly.
  • Secondary or Satellite TrPs arise in response to existing central trigger points in surrounding muscles. They usually spontaneously withdraw when the central TrP is healed. Can be present in form of a cluster.
Active AND Inactive /Latent Trigger Points
  • Active TrP is any point that causes tenderness and referral pain pattern on palpation. Almost always central TrPs are active and some satellite TrPs are also active (but non necessarily all of them). Inactive TrPs can evetually become active if there is a provocating factor.
  • Inactive or Latent TrPs can develop in anywhere and under fingertips feel like lumps, but are not painful. Can increase stiffness of the muscles.
Diffuse Trigger Points
  • Commonly happen in case of sever postural deformity where initially primary TrPs are multiple, so secondary multiple TrPs are only a response of a mechanism, called diffuse.
Attachment Trigger Points
  • Arise in tendo-osseouss junctions which become very tender. If not treated, degenerative processes of adjacent joint can spring up.
Ligamentous Trigger Points
  • Even ligaments can develop trigger points. Presence of TrPs in anterior longitudinal ligament of the spine can result in neck instability. Some knee pain syndrome are successfully healed when treated ligamentum patellae and fibular collateral ligament.

Pathogenesis[edit | edit source]

Little is known about the formation of TrPts, but these are probable theories; more research is necessary.[2][3][4][12][13]

There are some theories written in literature who try to explain the formation, sensitization and manifestation of TrPts, but few of them have strong evidence.

Several theories blame overuse in the development of TrPts. This could lead to endogenous (involuntary) shortening, loss of oxygen supply, loss of nutrient supply and increased metabolic demand on local tissues[2]. It is possible that abnormal depolarization of motor endplates and sustained muscular contraction give rise to a localized ‘ATP energy crisis’ associated with sensory and autonomic reflex arcs that are sustained by central sensitization[2] .This may occur due to a rise in the production and release of acetylcholine in motor endplate in resting state. This sustains the depolarization of muscle fiber which induces calcium releases. This gives the contraction with a lot of energy demand. This gives an energy crisis in the muscle fibers and impedes the calcium pump to return calcium. Then neuroactive substances create the sensitization of sensory and autonomic nerves which gives a rise of acetylcholine. These uncontrolled contractions explain the nodules and the sensitization could explain the pain. [5]

Under normal conditions, pain from TrPts is mediated by thin myelinated (Ad) fibres and unmyelinated (C) fibres. Various noxious and innocuous events, such as mechanical stimuli or chemical mediators, may excite and sensitize Ad fibres and C fibres and thereby play a role in the development of TrPs [2]

Other theories suggest that there are at least three pathophysiological processes that may be involved in the development and maintenance of
TrPts tendernes [4]. These include:
• sensitization of peripheral muscle nociceptors,
• sensitization of second-order neurons in the dorsal horn and in the trigeminal nucleus
• dysregulation of the descending endogenous pain control system.

Symptoms[edit | edit source]

  • motor dysfunctions,
  • muscle weakness or imbalance, altered motor recruitment , in either the affected muscle or in functionally related muscles
  • changes in Range of Motion (ROM),
  • painful movement,
  • tension headache,
  • tinnitus,
  • temporomandibular joint problems,
  • Pain when mechanically stimulated
  • Temporomandibular joitproblems when the TrPt are located in the jaw muscles
  • Postural abnormalities when they are located in the postural musculature.



Differential Diagnosis[edit | edit source]

The most important differential diagnosis is Tenderpoints.
Tenderpoints: Tender points, common in fibromyalgia, are discrete areas of tenderness over muscle, bone, tendon, and fat that cause local pain and are tender to palpation. Patients do not jump when tender points are palpated. Tender points do not refer pain to nearby or distant locations. [4]These two pain syndromes may overlap in symptoms and are difficult to differentiate without a thorough exam by a skilled physician. [3][8] (Level of evidence B)
Although they may be concomitant and may interact with one another.[8]

  1. Non-myofascial tenderpoints
  2. Musculoskeletal diseases:
    - Temporomandibular joint disorders
    - Occupational myalgias
    - Post-traumatic hyperirritability syndrome
    - Joint dysfunction (osteoarthritis)
    - Tendonitis and bursitis
  3.  Neurological disorders:
    - Trigeminal neuralgia
    - Glossopharyngeal neuralgia
    - Sphenopalatine neuralgia
  4. Systemic diseases
    - Rheumatoid arthritis
    - Gout
    - Psoriatic arthritis
    - Infections (viral, bacterial and/or protozoan)
  5. Heterotopic pain of central origion
  6. Axis II-type disorders
    - Psychogenic pain
    - Painful behaviors
    - Prug reactions

Diagnostic Procedures[edit | edit source]

Anamnesis and clinical examination

Anamnesis[edit | edit source]

Anamnesis (a patient's account of their own clinical history) should be specific. The patient must be asked about a diagnosis of Fibromyalgia or any relatives who were diagnosed whit Fibromyalgia. Furthermore, the therapist have to ask whether there is (chronic) muscle overuse, mechanical overload or repetitive microtrauma both in the present or the past. If not, the patient must be asked about his physical activities during the day. A lack of exercise may be a pathogenic factor. Work, work related psychological stress and possible sleep disturbances have to be asked. 

Examination[edit | edit source]

The study of trigger points can be recorded by palpation. Palpation of the TP will elicit pain and is harder than the “healthy” muscle. The pain perception may also be delayed a few seconds [4] 
There are also some specific signs seen in TrPts:
• Local twitch response
• Referred pain
• Motor dysfunctions,
 There has to be an Rom examination and Postural examination to check changes in Rom and posture.

• No laboratory test or imaging technique has been established for diagnosing TrPt[3]

Outcome Measures[edit | edit source]

Fischer has proposed the use of a pressure threshold meter (algometer), as a means of quantitative documentation of TrPt, and for quantifying the effects of the physical therapy treatment. Pressure pain threshold and visual analogue scale scores were the outcome measures more used in the analyzed trials. ROM also may be an outcome measurement for evaluating therapy. [13]

Medical Management[edit | edit source]

Neuroleptica and Local anesthtic injections [4], nsaid, antalgic painkillers[3]

Physical Therapy Management[edit | edit source]

There are several methods for the treatment of trigger points.

First the exact location of the trigger point should be palpated. Massage can cause the soft tissue back and that the different sarcomeres in the muscle of each other loose. [14] (Level of evidence 2b)

  •  Predisposing and perpetuating factors in chronic overuse or stress injury on muscles must be eliminated, if possible.[2]  the ethological factors offer an prolonged prognosis and have to be eliminated.[8](Level of evidence 2a)
  • ultrasonography, heath, ice, diathermy, tensare valuable in reducing pain and may inactivate TrPt [4][13] (Level of evidence A2)
  • Posture training and education about good and bad postures and initiate it in ADL and lifestyle [4] because lack of exercises and bad posture can provoke TrPts (Level of evidence 2c)
  • stretch of tight and shortened muscle
  • ischemic compression [13][8]and TrPt pressure release
    The terms “ischemic compression” and “myotherapy” have been used to describe treatment in which ischemia is induced in the TrPt zone by applying sustained pressure. However, this principle is questionable, since the nucleus of the trigger point intrinsically presents important hypoxia . Simons et al. described a similar treatment modality, though without the need to induce additional ischemia in the TrPt zone (TrPt pressure release). The aim of this technique is to free the contracted sarcomeres within the TrPt. The amount of pressure applied should suffice to produce gradual relaxation of the tension within the TrPt zone, without causing pain.[8] yet both techniques show imitate significant improvement of the ROM after treatment.[15][16]

Other managements[edit | edit source]

These are other possible therapies written in literature. Note: not all of theme have strong scientifically evidence. Lire research is necessary. A lot of the researches are not placebo-controlled and immediate effects after treatment may occur due to placebo-effects. . [13][8]

• acupunutre,
• dry needeling,
• Laser-therapy,
• ionophoresis.

Key Research[edit | edit source]

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Resources[edit | edit source]

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Clinical Bottom Line[edit | edit source]

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Recent Related Research (from Pubmed)[edit | edit source]

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References[edit | edit source]

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  1. ↑ 1.0 1.1 Simons DG, Travell JG, Simons LS. Travell & Simons' myofascial pain and dysfunction: upper half of body. Lippincott Williams & Wilkins; 1999.[1][2]
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Fernández-de-las-Peñas,C.etal. Myofascial trigger points and sensitization: an updated pain model for tension-type headache,Cephalalgia, 2007, 27, 383–393
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 DAVID J. ALVAREZ, Et al. Trigger Points: Diagnosis and Management, AMERICAN FAMILY PHYSICIAN 2002 , 65, 4, 653-660
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 Davidoff, RA. Trigger points and myofascial pain: toward understanding how they affect headachesCEPHALALGIA 1998,18, 436-448
  5. ↑ 5.0 5.1 5.2 Eduardo Vázquez Delgad, et al. Myofascial pain syndrome associated with trigger points: A literature review. (I): Epidemiology, clinical treatment and etiopathogeny Med Oral Patol Oral Cir Bucal. 2009 Oct 1;14 (10):494-498.
  6. ↑ Ray BS, Wolff HG. Experimental studies on headache: pain-sensitive structures of the head and their significance in headache. Archives of Surgery. 1940 Oct 1;41(4):813-56.[3]
  7. ↑ Niel-Asher S. The concise book of trigger points: a professional and self-help manual. North Atlantic Books; 2014.[4]
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 Eduardo Vázquez-Delgado. Et al. Myofascial pain associated to trigger points: A literature review. Part 2: Differential diagnosis and treatmentMed Oral Patol Oral Cir Bucal. 2010 Jul 1;15 (4):639-643
  9. ↑ Han SC, Harrison P. Myofascial pain syndrome and trigger-point management. Reg Anesth 1997;22: 89-101.
  10. ↑ Simons DG. Clinical and etiological update of myofascial pain from trigger points. Journal of musculoskeletal pain. 1996 Jan 1;4(1-2):93-122.[5]
  11. ↑ Simons DG, Travell JG, Simons LS. Travell & Simons’ Myofascial pain and dysfunction: the trigger point manual. 2d ed. Baltimore: Williams & Wilkins, 1999:11-93
  12. ↑ Elizabeth A. et al. Acupuncture and dry needling in the management of myofascial trigger point pain: A systematic review and meta-analysis of randomised controlled trials European Journal of Pain 13 (2009) 3–10
  13. ↑ 13.0 13.1 13.2 13.3 13.4 Fernandez de las Penas, C., et al. Manual therapies in myofascial trigger point treatment: a systimatic review: Journal of Bodywork and Movement Therapies (2005) 9, 27–34
  14. ↑ Arne, N., et al. ‘Treatment of myofascial trigger-points with ultrasound combined with massage and exercise – a randomised controlled trial’., 1998, 77 pg. 73-79
  15. ↑ Grieve R, et al. The immediate effect of soleus trigger point pressure release on restricted ankle joint dorsiflexion: A pilot randomised controlled trial. J Bodyw Mov Ther. 2011 Jan;15(1):42-49
  16. ↑ Montañez-Aguilera FJ. Et al. Changes in a patient with neck pain after application of ischemic compression as a trigger point therapy. J Back Musculoskeletal Rehabil. 2010;23(2):101-104.
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