트라벨 저서 TrP의 개요 - muscle pain의 이해를 위해서 반드시 공부해야

[문형철]

용어와 개념을 잘 알아야

활동성 발통점 또는 잠재성 발통점 기준

1. 긴장띠 촉진

2. 긴장띠 내에 예리한 spot tenderness

3. 활동성 tp의 통증성 nodule을 압박할때, 발생하는 통증을 환자가 지각

4. rom스트레칭시 통증성 제한

confirm‎atory observation

1. 국소적 연축반응을 보거나 촉지

2. tender nodule의 침자로 유발되는 국소적 연축반응 국소화

3. tender nodule의 압박시 통증이나 변화된 감각

4. 근전도로 관찰되는 자발성 활동전위

TrP의 임상적 특징

1. Taut band(nodule)안에서 spot tenderness는 근섬유의 촉진 가능한 tense band(긴장된 띠)가 있음.

2. 환자의 통증유발점에 압박을 주면 통증이 발생

3. 근육안에서 특징적인 통증유발점 패턴으로 통증이 전달

4. 국소연축반응(local twitch response)

5. 관절가동범위를 스트레칭시킬때 통증성 제한이 나타남

6. TrP에 의한 근력약화

TrP 존재검사법

1. 특수 근전도검사

2. 초음파

3. 표면근전도

4. 압박계

5. 온도 측정기 등

TrP의 적절한 치료법

1. 스트레칭

2. 근이완 테크닉

3. Injection

4. 통증유발점 영속화시키는 요인의 관리

5. 자가치료법

CLINICAL CHARACTERISTICS OF TRIGGER POINTS (Section B) are a history of pain related to muscular activity and characteristic physical findings. Examination of the muscle reveals circumscribed spot tenderness in a nodule that is part of a palpably tense band of muscle fibers, patient recognition of the pain evoked by pressure on the tender spot as being familiar, pain referred in the pattern characteristic of TrPs in that muscle, a local twitch response (LTR), painful limitation of stretch range of motion, and some weakness of that muscle. 

Promising TESTING methods that demonstrate the presence of TrPs include a specific needle electromyographic(EMG) technique, ultrasound, surface EMG, algometry, and thermography. Referred motor dysfunctions during activity can be tested using surface EMG techniques. 

Appropriate TREATMENT of patients for TrPs may involve many forms of stretch, several techniques to augment muscle

release, injection of TrPs, management of perpetuating factors, and a home self-treatment program.

chapter 9. Muscles and Muscle Tissue.pdf

통증유발점의 활동성 부위(active locus of trigger point) : 자발적인 전기활동을 보이는 미세한 근육부위.

A minute region in a muscle that exhibits spontaneous electrical activity (often characterized as endplate noise) and that may or may not also exhibit spike activity characteristic of single fiber action potentials.  

활동성 근막통 유발점(active myofascial trigger point) : 임상적인 통증을 유발하는 근막 통증지점으로 항상 통증(tender)이 있고, 근육의 완전신장을 방해하고, 근력약화를 야기, 직접 압박(direct compression)에 환자는 통증으로 인지하고, 적절한 자극을 받을때 근섬유는 국소적 연축(local twitch) 반응을 보임. 환자의 통증 내성내에서 압박될때는 통증 연관통 범위내에 referred motor phenomena가 생성되고, 때로는 자율신경 반응(autonomic phenomena)이 발생하고, 통증 연관지역내에서 tenderness 를 야기함.  

A myofascial trigger point that causes a clinical pain complaint. It is always tender, prevents full lengthening of the muscle, weakens the muscle, refers a patient-recognized pain on direct compression, mediates a local twitch response of muscle fibers when adequately stimulated, and, when compressed within the patient's pain tolerance, produces referred motor phenomena and often autonomic phenomena, generally in its pain reference zone, and causes tenderness in the pain reference zone.

연관근막통 유발점(associated myofascial trigger point) :  다른 근육에 발통증을 동시에 동반하는 근육내 발통점. 이러한 연관근육발통점 중 한 곳이 다른 부위에 통증을 유발키기도 함. 이 두 부위가 모두 같은 기계적 또는 신경학적 근원에서 발현될 수 있음. 

A trigger point in one muscle that occurs concurrently with a trigger point in another muscle. One of these associated

trigger points may have induced the other, or both may stem from the same mechanical or neurologic origin. 

부착부 통증유발점(attachment trigger point) :  근건접합부 또는 건뼈접합부의 발통점으로 중심부 발통점에 의해서 생성된 단단한 띠가 치료되지 않아서 발생함. 

A trigger point at the musculotendinous junction and/or at the osseous attachment of the muscle that identifies the enthesopathy caused by unrelieved tension characteristic of the taut band that is produced by a central trigger point.

중심부 통증유발점(central myofascial trigger point) : 근섬유의 중심 또는 중심근처부위의 기능장애가 있는 종판과 밀접하게 연관된 근막발통점

A myofascial trigger point that is closely associated with dysfunctional endplates and is located near the center of muscle fibers.

Enthesitis: "Traumatic disease occurring at the insertion of muscles where recurring concentration of muscle stress provokes inflammation with a strong tendency toward fibrosis and calcification."7 The enthesopathy referred to in this book may, in time, develop into an enthesitis.

Enthesopathy: A disease process at musculotendinous junctions and/or where tendons and ligaments attach into bones or joint capsules. It is characterized by local tenderness and may, in time, develop into enthesitis.

근본통증 부위(essential pain zone) ; 통증패턴그림에서 굵은 붉은색으로 표시되는 연관통부위로 통증유발점이 활성일때, 거의 모든 환자에서 존재함. 과잉연관통부위와 구별되어야

The region of referred pain (indicated by solid red areas in pain pattern figures) that is present in nearly every patient when the trigger point is active. To be distinguished from a spillover referred pain zone.

Joint Play: Small movements within a synovial joint that are independent of, and cannot be induced by, voluntary muscle

contraction. Essential for normal, pain-free, nonrestricted movement of the articulation.2

Jump Sign: A general pain response of the patient, who winces, may cry out, and may withdraw in response to pressure applied on a trigger point. This term has been used erroneously to describe the local twitch response of muscle fibers to trigger-point stimulation.

핵심 근막통 유발점(Key Myofascial Trigger Point): 활성화된 하나 또는 좀더 많은 위성 발통점을 유발하는 핵심 근막발통점. 임상적으로 핵심 발통점을 비활성화 시키면 위성발통점도 함께 비활성화 됨. 

 A trigger point responsible for activating one or more satellite trigger points. Clinically, a key trigger point is identified when inactivation of that trigger point also inactivates the satellite trigger point.

잠복성 근막통 유발점(latent myofascial trigger point) : 자발적인 통증과 연관된 임상적으로 정지되어 있는 근막통 유발점. 촉진시에만 통증이 있음. 잠복성 근막통유발점은 활동성 통증유발점의 모든 임상적 특징을 다 가지고 있으며, 항상 근긴장을 증가시키고 운동가동범위를 제한하는 단단한 띠를 가지고 있음. 

A myofascial trigger point that is clinically quiescent with respect to spontaneous pain; it is painful only when palpated. A latent trigger point may have all the other clinical characteristics of an active trigger point and always has a taut band that increases muscle tension and restricts range of motion

국소연축반응(local twitch response) : 통증 유발점을 가로지르는 단단한 띠의 일시적인 수축같은 통증유발점. 때로는 통증유발점 인접부의 자극에 반응하는 근섬유들의 수축. 때로 국소연축반응은 점프징후로 오인되기도 함. 

A transient contraction of a group of tense muscle fibers (taut band) that traverse a trigger point. The contraction of the fibers is in response to stimulation (usually by snapping palpation or needling) of the same trigger point, or sometimes of a nearby trigger point. Sometimes the local twitch response has been erroneously called a jump sign.

Myofascial Pain Dysfunction Syndrome: A controversial, largely outmoded term that has been considered to mean a syndrome largely of muscular origin, a complex psychophysiological phenomenon, or a syndrome primarily due to disturbed occlusal mechanics.

Myofascial Pain Syndrome (Myofascial Syndrome): 

1. (as used in this book) The sensory, motor, and autonomic symptoms caused by myofascial trigger points. The specific muscle or muscle group that causes the symptoms should be identified. 

2. (as sometimes confusingly used by others) A regional pain syndrome of any soft tissue origin.To avoid confusion, we recommend that when anyone uses the term myofascial pain syndrome, that person should specify which meaning applies. file general or specific definition.

Myofascial Trigger Point (clinical definition of a central trigger point): A hyperirritable spot in skeletal muscle that is associated with a hypersensitive palpable nodule in a taut band. The spot is painful on compression and can give rise to characteristic referred pain, referred tenderness, motor dysfunction, and autonomic phenomena. Types of myofascial trigger points include: active, associated, attachment, central, key, latent, primary, and satellite. (Note  especially the distinction between central and attachment myofascial trigger points). Any myofascial trigger point is to be distinguished from a cutaneous, ligamentous, periosteal, or any other nonmuscular trigger point.

Myofascial Trigger Point (etiological definition of a central trigger point): A cluster of electrically active loci each of which is associated with a contraction knot and a dysfunctional motor endplate in skeletal muscle.

일차성근막통유발점(Primary Myofascial Trigger Point) : 급성 또는 만성, 반복적인 근육의 사용으로 인해 명백하게 활성회되는 중심부근막통 유발점으로 다른 근육 통증유발점의 활성화에 의한 결과로 생기지 않음. 

A central myofascial trigger point that was apparently activated directly by acute or chronic overload, or repetitive overuse of the muscle in which it occurs and was not activated as a result of trigger-point activity in another muscle.

위성근막통유발점(Satellite Myofascial Trigger Point): 핵심 통증유발점 활성에 의해서 신경학적 또는 기계적으로 유도된 중심부 근막통 유발점. 핵심-위성의 관계를 규정짓는 기전의 구분은 검사자체만으로는 알수없음. 그 관계는 일반적으로 핵심 통증유발점이 비활성화되었을때, 위성통증유발점도 비활성화된 것을 봄으로써 동시에 확인할 수 있음. 통증 유발점은 중심부 통증유발점의 연관부위에서 생기게 되며 중심부 통증유발점이 있는 근육을 대신하여 과부하된 협동근에 생김. 중심근의 증가된 긴장을 받는 길항근에 생기기도 하며, 중심부 통증유발점에 명확하게 신경학적으로만 연결되어 있는 근육에도 생길 수 있음. 

A central myofascial trigger point that was induced neurogenically or mechanically by the activity of a key trigger point. Distinguishing the mechanism responsible for the key-satellite relationship can rarely be resolved by examination alone. The relationship usually is confirmed by simultaneous inactivation of the satellite when the key trigger point is inactivated. A satellite trigger point may develop in the zone of reference of the key trigger point, in an overloaded synergist that is substituting for the muscle harboring the key trigger point (key muscle), in an antagonist countering the increased tension of the key muscle, or in a muscle linked apparently only neurogenically to the key trigger point. Previously, only a trigger point that developed in the referred pain zone of another trigger point was identified as a satellite trigger point.

이차성통증유발점(Secondary Trigger Point) : 예정에 많이 사용되었지만 본책에서는 거의 사용하지 않음. 예전에 이차성 통증유발점으로 정의되어지던 것은 현재는 위성통증유발점으로 분류되어짐. 이차성 통증유발점은 예전에는 핵심 통증유발점을 가지고 있는 근육의 협력근 또는 길항근에서 생기는 것으로 인정됨. 

Term previously used, but rarely in this edition. Trigger points previously identified as secondary trigger points are now classified as satellite trigger points. A secondary trigger point was previously identified as one that developed in a synergist or an antagonist of the muscle harboring the key trigger point.

Referred Autonomic Phenomena: Vasoconstriction(blanching), coldness, sweating, pilomotor response, ptosis, and/or hypersecretion that occur in a region separate from the trigger point causing these phenomena. The phenomena usually appear in the same general area to which that trigger point refers pain.

Referred (Trigger-Point) Pain: Pain that arises in a trigger point, but is felt at a distance, often entirely remote from its

source. The pattern of referred pain is reproducibly related to its site of origin. The distribution of referred trigger-point pain rarely coincides entirely with the distribution of a peripheral nerve or dermatomal segment.

Snapping Palpation: A fingertip is placed against the tense band of muscle at right angles to the direction of the band and suddenly presses down while the examiner draws the finger back so as to roll the underlying fibers under the finger. (The motion is similar to that used to pluck a guitar string, except that the finger does not slide over the skin but moves the skin with it.) To most effectively elicit a local twitch response, the band is palpated and snapped at the trigger point, with the muscle positioned to eliminate slack. To be distinguished from flat palpation and pincer palpation.

긴장 띠(Taut Band) : 통증유발점으로부터 근육의 부착부까지 확장되어 있는 긴장된 근섬유들의 그룹. 근섬유들의 긴장은 통증유발점에 위치하고 잇는 수축매듭에 의해서 생기게 됨. 이러한 띠 내에 있는 근섬유들의 반사성 수축으로 국소 연축반응이 생김.

The group of tense muscle fibers extending from a trigger point to the muscle attachments. The tension of the fibers is caused by contraction knots that are located in the region of the trigger point. Reflex contraction of the fibers in this band produces the local twitch response.

TrP의 유병률

Myofascial trigger points (TrPs) are extremely common and become a painful part of nearly everyone's life at one time or

another. Latent TrPs, which often cause motor dysfunction (stiffness and restricted range of motion) without pain, are far more common than the active TrPs, which in addition cause pain.

TrP 근막통유발점은 너무도 흔해서 일생동안 한번 이상나타남. 

잠복성 근막통유발점은 흔히 통증을 유발하지 않고, 경직이나 운동범위제한과 같은 운동기능이상을 초래하며, 통증을 유발하는 활동성 근막통유발점보다 흔함. 

Among 200 unselected, asymptomatic young adults, Sola, et a/.2 6 1 found focal tenderness representing latent TrPs in the shoulder-girdle muscles of 54% of the female, and 4 5% of the male subjects. Referred pain was demonstrated in 25% of these subjects with latent TrPs. 

증상이없는 성인 200명의 어깨견갑대 근육의 근막통유발점을 조사한 결과.

여자의 54%, 남자의 45%에서 잠복성 근막통유발점을 발견함. 

A recent study of 269 unselected female student nurses with or without pain symptoms2 2 8 showed a similar high  preval‎ence of TrPs in masticatory muscles. A TrP was identified by palpating a taut band for spot tenderness of sufficient sensitivity to cause a pain reaction. No effort was made to distinguish active and latent TrPs, but a considerable number of TrPs were likely active because 28% of subjects were aware of pain in the temple area. In masticatory muscles, TrPs were found in 54% of right lateral pterygoid muscles, in 45% of right deep masseter, in 4 3% of right anterior temporalis, and in 40% of intraoral examinations of the right medial pterygoid muscle. Among the neck muscles, TrPs were identified in 35% of the right splenius capitis muscles and in 33% of right upper trapezius muscles. The insertion of the right upper

trapezius was also tender in 42% of those muscles with TrPs. Enthesopathy of this muscle was common.2 2 8

Frohlich and Frohlich8 4 examined 100 asymptomatic control subjects for latent TrPs in lumbogluteal muscles. They found

latent TrPs in the following muscles: quadratus lumborum (45% of patients), gluteus medius (41%), iliopsoas (24%), gluteus minimus (11%), and piriformis (5%). Reports of the preval‎ence of myofascial TrPs in specific patient populations are available and, together, indicate a high preval‎ence of this condition among individuals with a regional pain complaint. The reports that follow are summarized in Table 2.1.

증상이 없는 100명 허리와 엉덩이 근육에서 잠재성 발통점 연구

요방형근 45%, 중둔근 41%, 장요근 24%, 소둔근 11%, 이상근 5%.

In an internal medicine group practice, 54 of 172 patients presented with a pain complaint. Sixteen [30%] of the pain

patients met the criteria for myofascial TrPs. Four of these sixteen patients had pain duration of less than 1 month, three had pain for 1 to 6 months, and nine had pain duration of more than 6 months. A neurologist examining 96 patients from a community pain medical center90 found that 93% had at least part of their pain caused by myofascial TrPs and in 74%, myofascial TrPs were considered the primary cause of the pain.

내과환자의 경우 172명중 54명이 통증 호소. 그중 30%이 근막성 발통점.

Among 283 consecutive admissions to a comprehensive pain center, a primary organic diagnosis of myofascial syndrome was

assigned in 85% of cases.80 A neurosurgeon and a physiatrist made this diagnosis independently, based upon physical examination "as described by Simons and Travell."255 Of 164 patients referred to a dental clinic for chronic head and neck pain of at least 6 months duration, 55% were found to have a primary diagnosis of myofascial pain syndrome caused by active TrPs.83

Five lumbogluteal muscles of 97 patients complaining of pain in the locomotor system were examined in an orthopedic clinic.84 Forty-nine percent of the patients presented with latent TrPs and 2 1% presented with active TrPs in the piriformis muscle.

The wide range in preval‎ence of myofascial pain caused by TrPs that is reported in different studies is likely due in part to

differences in the patient populations examined and in the degree of chronicity. 

Probably even more important are differences in the criteria used to make the diagnosis of myofascial TrPs and, most important, differences in the training and skill level of the examiners. Few of these studies gave a detailed description of the diagnostic examinations employed. A summary of preval‎ence2 4 2 excluded papers that used the general definition241 of a myofascial pain syndrome. 

Active myofascial  TrPs are clearly very common and are a major source of musculoskeletal pain and dysfunction, but poor agreement on appropriate diagnostic criteria has been a serious handicap. A study has critically tested interrater reliability for 5 manual examinations in 5 different muscles9 4 among four experienced and trained examiners. The study demonstrated good to excellent agreement for all muscles and for all examinations except for one examination, which was not highly reliable for all muscles tested.

In a population of hospitalized and ambulatory Physical Medicine and Rehabilitation Service patients with the fibrositis syndrome (mostly TrPs), the greatest number were between 31 and 50 years of age.1 5 5 These data agree with our clinical impression that individuals in their mature years of maximum activity are most likely to suffer from the pain syndromes of active myofascial TrPs. With the reduced activity of more advanced age, the stiffness and restricted range of motion

of latent TrPs tend to become more prominent than the pain of active TrPs.

근막통증후군의 severity

The severity of symptoms caused by myofascial TrPs ranges from the agonizing incapacitating pain caused by

very active TrPs to the painless restriction of movement and distortion of posture due to latent TrPs that are so commonly overlooked.

Trp로 인한 증상은 활동성 발통점으로 야기되는 참을수 없는 통증, 무능력하게 하는 정도의 통증으로부터 잠재성 통증으로야기되는 무통증성 움직임 제한과 자세 왜곡 등 넓은 범위에 걸쳐있음. 

TrP 발통점의 임상적 특징

Active TrPs produce a clinical complaint (usually pain) that the patient recognizes when the TrP is digitally compressed. Latent TrPs can produce the other effects characteristic of a TrP including increased muscle tension and muscle shortening (but do not produce spontaneous pain). 

Both active and latent TrPs can cause significant motor dysfunction. It appears that the same factors which are responsible for the development of an active TrP, to a lesser degree, can cause a latent TrP. An active key TrP in one muscle can induce an active satellite TrP in another muscle. Inactivation of the key TrP often also inactivates its satellite TrP without treatment of the satellite TrP itself.

활동성 tp는 임상적으로 통증으로 호소되며, tp를 압박했을때 이를 인지함. 

잠재성 tp는 근긴장도 증가, 근육단축(하지만 자발적인 통증은 없음). 

활동성, 잠재성 tp는 모두 심각한 움직임 기능부전을 초래할 수 있음. 

같은 원인이 잠재성, 활동성 tp를 만들어내는데, 약한 요인일때 잠재성 tp가 만들어짐. 

한 근육에서 핵심 활동성 tp는 활동성 위성 tp를 유도할 수 있음. 핵심 활동성 tp를 불활성화 시키면 위성 tp는 치료하지 않아도 불활성화 됨. 

발통점의 발현

The activation of a TrP is usually associated with some degree of mechanical abuse of the muscle in the form of muscle overload, which may be acute, sustained, and/or repetitive. In addition, leaving the

muscle in shortened position can convert a

latent TrP to an active TrP and this process is

greatly aggravated if the muscle is contracted

while in the shortened position. In

paraspinal (and very likely other) muscles, a

degree of nerve compression that causes

identifiable neuropathic electromyographic

changes is associated with an increase in the

numbers of active TrPs.3 7 These TrPs may be

activated by disturbed microtubule communication

between the neuron and the endplate

since the motor endplate is the peripheral

core TrP pathophysiology.

The patient is aware of the pain caused

by an active TrP but may or may not be

aware of the dysfunction it causes. Latent

TrPs characteristically cause some increased

muscle tension and limitation of

stretch range of motion, which often escapes

the patient's attention or is simply

accepted. The patient becomes aware of

pain originating from a latent TrP only

when pressure is applied to it. Spontaneous

referred pain appears with increased

irritability of the TrP, and it then is identified

as active.1 2 5

The patient usually presents with complaints

due to the most recently activated

TrP. When this TrP has been successfully eliminated, the pain pattern may shift to

that of an earlier, key TrP which also must

be inactivated. If the key TrP is inactivated

first, the patient may recover without further

treatment.

The intensity and extent of the referred

pain pattern depends on the degree of irritability

of the TrP, not on the size of the

muscle. Myofascial TrPs in small, obscure,

or variable muscles can be as troublesome

to the patient as TrPs in large familiar

muscles.

As illustrated in Figure 2.1, trigger

points are activated directly by acute overload,

overwork fatigue, direct impact

trauma, and by radiculopathy.

Trigger points can be activated indirectly

by other existing TrPs, visceral disease,

arthritic joints, joint dysfunctions, and by

emotional distress. Satellite TrPs are prone to

develop in muscles that lie within the pain

reference zone of key myofascial TrPs, or

within the zone of pain referred from a diseased

viscus, such as the pain of myocardial

infarction, peptic ulcer, cholelithiasis, or renal

colic. A perpetuating factor (see Chapter

4) increases the likelihood of overload stress

converting a latent TrP to an active TrP.

With adequate rest, and in the absence

of perpetuating factors, an active TrP may

revert spontaneously to a latent state. Pain

symptoms disappear, but occasional reactivation

of the TrP by exceeding that muscle's

stress tolerance can account for a history

of recurrent episodes of the same pain

over a period of years.

Onset. The activation of a TrP is usually associated with some degree of mechanical abuse of the muscle in the form of muscle overload, which may be acute, sustained, and/or repetitive. In addition, leaving the muscle in shortened position can convert a latent TrP to an active TrP and this process is greatly aggravated if the muscle is contracted while in the shortened position. In paraspinal (and very likely other) muscles, a degree of nerve compression that causes identifiable neuropathic electromyographic changes is associated with an increase in the numbers of active TrPs.3 7 These TrPs may be activated by disturbed microtubule communication between the neuron and the endplate since the motor endplate is the peripheral core TrP pathophysiology.

The patient is aware of the pain caused by an active TrP but may or may not be aware of the dysfunction it causes. Latent

TrPs characteristically cause some increased muscle tension and limitation of stretch range of motion, which often escapes the patient's attention or is simply accepted. The patient becomes aware of pain originating from a latent TrP only

when pressure is applied to it. Spontaneous referred pain appears with increased irritability of the TrP, and it then is identified as active.1 2 5

The patient usually presents with complaints

due to the most recently activated

TrP. When this TrP has been successfully eliminated, the pain pattern may shift to

that of an earlier, key TrP which also must

be inactivated. If the key TrP is inactivated

first, the patient may recover without further

treatment.

The intensity and extent of the referred

pain pattern depends on the degree of irritability

of the TrP, not on the size of the

muscle. Myofascial TrPs in small, obscure,

or variable muscles can be as troublesome

to the patient as TrPs in large familiar

muscles.

As illustrated in Figure 2.1, trigger

points are activated directly by acute overload,

overwork fatigue, direct impact

trauma, and by radiculopathy.

Trigger points can be activated indirectly

by other existing TrPs, visceral disease,

arthritic joints, joint dysfunctions, and by

emotional distress. Satellite TrPs are prone to

develop in muscles that lie within the pain

reference zone of key myofascial TrPs, or

within the zone of pain referred from a diseased

viscus, such as the pain of myocardial

infarction, peptic ulcer, cholelithiasis, or renal

colic. A perpetuating factor (see Chapter

4) increases the likelihood of overload stress

converting a latent TrP to an active TrP.

With adequate rest, and in the absence

of perpetuating factors, an active TrP may

revert spontaneously to a latent state. Pain

symptoms disappear, but occasional reactivation

of the TrP by exceeding that muscle's

stress tolerance can account for a history

of recurrent episodes of the same pain

over a period of years.

Pain Complaint. Patients with active

myofascial TrPs usually complain of

poorly localized, regional, aching pain in

subcutaneous tissues, including muscles

and joints. They rarely complain of sharp,

clearly-localized cutaneous-type pain. The

myofascial pain is often referred to a distance

from the TrP in a pattern that is characteristic

for each muscle. Sometimes the

patient is aware of numbness or paresthesia

rather than pain.

Infants have been observed with point

tenderness of the rectus abdominis muscle

and colic, both of which were relieved by sweeping a stream of vapocoolant over the

muscle, which helps to inactivate myofascial

TrPs.

When children with musculoskeletal

pain complaints were examined for myofascial

TrPs, the TrPs were found to be a

common source of their pain.1 2 It is our impression

that the likelihood of developing

pain-producing active TrPs increases with

age into the most active, middle years. As

activity becomes less strenuous in later

years, individuals are more likely to be

aware of the stiffness and restricted motion

resulting from latent TrPs.

Sola2 5 9 found that laborers who exercise

their muscles heavily every day, are less

likely to develop active TrPs than are

sedentary workers who are prone to intermittent

orgies of vigorous physical activity.

Our clinical experience has been similar.

Active TrPs are found commonly in postural

muscles of the neck, shoulder and

pelvic girdles, and in the masticatory muscles.

In addition, the upper trapezius, scalene,

sternocleidomastoid, levator scapulae

and quadratus lumborum muscles are

very commonly involved.

Dysfunctions. In addition to the clinical

symptoms produced by the sensory disturbances

of referred pain, dysesthesias,

and hypesthesias, patients also can experience

clinically important disturbances of

autonomic and motor functions.

Disturbances of autonomic functions

caused by TrPs include abnormal sweating,

persistent lacrimation, persistent coryza,

excessive salivation, and pilomotor activities.

Related proprioceptive disturbances

caused by TrPs include imbalance, dizziness,

tinnitus, and distorted weight perception

of lifted objects.

Disturbances of motor functions caused

by TrPs include spasm of other muscles,

weakness of the involved muscle function,

loss of coordination by the involved muscle,

and decreased work tolerance of the

involved muscle. The weakness and loss of

work tolerance are often interpreted as an

indication for increased exercise, but if this

is attempted without inactivating the responsible

TrPs, the exercise is likely to encourage

and further ingrain substitution by

other muscles with further weakening and

deconditioning of the involved muscle.

The combination of weakness in the hands

and loss of forearm muscle coordination

makes grasp unreliable. Objects sometimes

slip unexpectedly from the patient's grasp.

The weakness results from reflex motor inhibition

and characteristically occurs without

atrophy of the affected muscle. The patient

is prone to substitute intuitively

without realizing that, for instance, he or

she is carrying the grocery bag in the nondominant

but now-stronger arm.

The motor effects of TrPs on the muscle

in which the TrPs are located are considered

in detail below under Surface EMG.

Sleep Disturbances. Disturbance of

sleep can be a problem for patients with a

painful TrP syndrome. Moldofsky1 9 6 has

shown in a series of studies that many sensory

disturbances, including pain, can seriously

disturb sleep. This sleep disturbance

can, in turn, increase pain sensitivity the

next day. Active myofascial TrPs become

more painful when the muscle is held in

the shortened position for long periods of

time and also if body weight is compressing

the TrP. Thus, for patients with active

TrPs, sleep positioning can be critical to

avoid unnecessarily disturbing their sleep. 

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trp의 개요. 감사합니다