Bluegrass Doctors of
Physical Therapy, PLLC
Bluegrass Doctors of
Physical Therapy, PLLC
|Posted on August 13, 2015 at 8:45 AM|
Do you Suffer with Ringing in the ears? (AKA Tinnitus). Have you had a myriad of tests only to find no cause for your symptoms? That feeling in your ear may be coming from a muscle. Believe it or not!
Lets dive a little deeper.
The muscles of the head and neck were neglected as a cause of medical problems until Dr. Janet Travell described myofascial dysfunction (MFD). The tenets of MFD are described in the classic Travell-Simons text- book, Myofascial Pain and Dysfunction: The Trigger Point Manual (1). MFD is a primary muscle disorder which is characterized by: a) taut bands (tight bands of contracted muscle fibers), trigger points (TrPs, exquisitely tender, discrete nodule within the taut bands), muscle shortening and muscle stiffening, with attendant limitation of range of motion, motor abnormalities, and disturbed motor function; b) sensory abnormalities, such as tenderness and referred symptoms; c) autonomic changes which are occasionally present, especially in longstanding cases.
MFD develops as a result of muscle abuse in in- dividuals who have a poorly understood predisposition to this disorder. The muscle abuse takes the form of: a) overuse (e.g. sitting for many hours with poor posture, and other poor work ergonomics); b) misuse (e.g. para- functional chewing due to a dental problem); c) under- use; d) trauma (e.g. whiplash). Chronic tightening of the upper shoulder muscles from mental stress also plays a role. Other factors which promote myofascial dysfunction are metabolic, endocrine, and nutritional abnormalities. (These factors along with the muscle abuse factors are known as precipitating and perpetuating factors. The muscle abuse types of precipitating and perpetuating factors may not be readily apparent). There is a female: male incidence of MFD on the order of 3:1 to 9:18. Muscles involved with MFD can cause local or referred symptoms, or can incite secondary trigger points (termed satellite trigger points) which can in turn themselves cause local or referred symptoms. Although pain is the best known symptom of this muscle disorder, MFD is responsible for a large number and a wide variety of symptoms, especially in the head and neck. These symptoms often masquerade as primary disorders of the ear, nose, and throat. One of these symptoms is tinnitus. The influence of the musculoskeletal system upon certain types of tinnitus is well recognized.
Tinnitus of myofascial origin may be unilateral or bilateral. There are no predictive audiometric patterns for MFD tinnitus. Patients with severe hearing loss may completely clear their tinnitus with MFD treatment, and tinnitus sufferers with a normal audiogram may have no improvement with MFD treatment, and vice versa. Although there is no strong predictor of which patients will benefit from MFD treatment, the following factors are somewhat more predictive of a favorable outcome:
1. Tinnitus which has been present for a shorter period — e.g. under 2 years vs. 10-20 years.
2. Tinnitus which accompanies other myofascial ENT/head & neck symptoms.
3. Tinnitus which fluctuates in intensity synchronously with other myofascial ENT/head and neck symptoms.
4. Tinnitus which is more pronounced on the side ipsilateral (or on the same side) to the more prominent accompanying myofascial symptoms.
Sound like any of your symptoms? If you have these symptoms and all other patholgoy has been ruled out, don't give up! We can help!!! Give us a call at 1-502-771-1774. Your symptoms may be muscular in origin and can oftem be alleviated in 2-4 treatments!
|Posted on June 3, 2015 at 10:10 PM|
What Your Cardiologist Should Know About FMS and CMP
There are many symptoms that can lead the person with fibromyalgia syndrome (FMS) and/or chronic myofascial pain (CMP) to your office. Research is pointing to FMS as a sympathetically-maintained disorder of pain processing (Martinez-Lavin, Vidal, Barbosa et al. 2002) and a form of dysautonomia (Raj, Brouillard, Simpson et al 2000). Chronic myofascial pain can mimic or accompany cardiovascular disease (Simons, Travell and Simons 1999). You need to be familiar with the myofascial trigger points (TrPs). Both FMS and CMP work together to create a symptom load greater than the sum of the two and may present a picture perplexing to the diagnostician.
Research indicates that fibromyalgia may increase the risk of cardiovascular disease (Curtis, O’Keefe Jr 2002). Intracellular calcium concentrations may be significantly reduced in fibromyalgia patients (Magaldi, Moltoni, Biasi et al 2000), and we don’t yet know how this may interrelate with the excess calcium release at the motor endplates in the area of myofascial TrPs (Simons, Travell and Simons, 1999). Research has shown an abnormal autonomic response to orthostatic stress in men with FMS (Cohen, Neumann, Alhosshle et al. 2001). Nail ridges or beads, fragile nails and clubbing (beaking) of nails are common in FMS. This may be associated with chronic lack of oxygen due to TrPs in the respiratory muscles, neurotransmitter or endocrine dysfunction of FMS, or weakened respiratory muscle strength due to FMS (Ogzocmen, Cimen, Ardicoglu 2002).
The dysregulation of neurotransmitters in FMS can lead to a drop in hemoglobin oxygenation during sleep (Alvarez Lario, Alonso Valdivieso, Alegre Lopez, et al. 1996). Constricted bronchi caused by neurotransmitter dysregulation may contribute. In FMS, neurotransmitter dysfunction often has a direct impact on the cardiovascular system. Research has shown that chronic dyspnea not due to cardiac or pulmonary causes is common in people with chronic primary FMS (Caidahl, Lurie, Bake, et al. 1989).
Neurally mediated hypotension is often a frightening and potentially dangerous companion to FMS (Bou-Holaigah, Calkins, Flynn, et al. 1997; Clauw 1995). There is also an increase in mitral valve prolapse (Pellegrino, Van Fossen, Gordon, et al. 1989). Expect dyspnea (Weiss, Kreck and Albert 1998; Caidahl, Lurie, Bake, et al. 1989). The combination of these and other symptoms can be frightening and add to your patient's stress. Check everything out, but reassure your patient that these can co-exist with FMS. You may want to prepare a handout with a list of warning signs that should be reported. Treating the co-existing myofascial TrPs may save you many needless calls and save your patients unnecessary trips to the ER.
Shortness of breath is often due to TrPs in the serratus anterior muscle and is commonly associated with a "stitch in the side". There is referred pain to the side and to the back of the chest. This includes the lower interior border of the shoulder blade, and sometimes runs down the inner area of the arm, hand, and the last two fingers. There may be air hunger, with panting or mouth breathing. In severe cases, there is chest pain even at rest. The nerve going to the serratus anterior muscle may be entrapped because of scalene muscle TrPs. This TrP can also contribute substantially to the pain of a heart attack (Simons, Travell and Simons 1999). It can also cause a catch in the lower inner side of the shoulder blade. Serratus posterior inferior TrPs produce an unusual ache radiating over and around the muscle. Ilicostalis thoracis TrPs at mid-chest level send pain upward toward the shoulder as well as sideways toward the chest wall. Trigger points on the left side in this area cause pain that is often mistaken for angina.
Restricted chest expansion causes less air to be taken into the lungs. Researchers report that maximum expiratory and inspiratory pressures are low in chronic primary FMS, which may indicate respiratory muscle dysfunction (Lurie, Caidahl , Johansson et al. 1990). Levator scapulae TrPs can also cause shortness of breath (Neoh 1995). If your patient has a stiff neck as well, look for these TrPs.
If the tissues surrounding the carotid sinuses harbor TrPs, their ability to control the blood pressure by constricting and dilating the blood vessels could be affected. Neurotransmitter imbalances of FMS may also be a part of fluctuating blood pressure. Chronic pain itself can affect blood pressure (Nilsson, Kandell-Collen, Andersson, 1997), and it is vital that this symptom be kept under control. Metabolic Syndrome is a frequent perpetuating factor of both FMS and CMP, so monitor your patient’s cholesterol levels, abdominal obesity and possible insulin resistance. TrPs can cause entrapment of blood and lymph vessels. This can cause swelling and can affect the blood pressure. High blood pressure can also aggravate scalene TrPs, causing a mutual aggravation spiral.
All major scalene muscles can refer pain to the front and back of the body in a widespread pattern. In the front they cause persistent aching pain over the chest and down the front and back of the arm to the forearm. The patient may tell you that the chest feels tight. On the left side, this pain may be mistaken for angina. Shallow pain also can be referred to the inner-upper border of the shoulder blade. There may be signs showing obstruction of veins and arteries and compression of the motor and sensory nerves of the arm. Sleep is often disturbed by pain from these TrPs. Your patient may have to sleep sitting up or propped up on pillows. There may be numbness, tingling, and odd sensations in the fourth and fifth fingers and in the little finger side of the hand and forearm.
Intercostal TrPs cause aching pain primarily locally. Palpate for these TrPs around the ribs. They are most often located on the front of the body, close to the side. Your patient may not be able to endure pressure on these TrPs. The pain increases when s/he takes a deep breath, coughs or sneezes. In the area near the breastbone, these TrPs may cause cardiac arrhythmia (Simons, Travell and Simons, 1999, p 875).
Diaphragm TrPs refer pain in two different directions, using two different neural pathways. One sends pain to the upper border of the shoulder on the same side as the TrP, from TrPs in the diaphragm dome. TrPs along the edges send pain to the edges of the ribs close by. Diaphragm TrPs can cause the "stitch in the side", chest pain, or inability to get a full breath. The pain will be most intense on exhalation after a deep breath. These TrPs cause restricted rotation of the spine upon twisting to look behind. Chronic cough, paradoxical breathing will perpetuate these TrPs, as will head-forward, slumped-shouldered posture. Local impact trauma, chest surgery (chest retractors are likely to leave clusters of TrPs in their wake), herpes zoster, rib fractures are also possible initiating and perpetuating factors, as are tumors, and some repetitive exercises.
There may be a TrP on the right side pectoralis major between the 5th and 6th ribs about midway between the nipple and the outer edge of the sternum that can be involved with cardiac arrhythmias. Treating the TrP may eliminate the arrhythmia. Pectoralis major TrPs cause pain under the sternum. They also can transmit pain to the front of the chest and breast, extending down to the little finger side of the arm to the fourth and fifth fingers. TrPs on the left side often mimic heart-attack pain.
Pectoralis TrPs can occur in any of the muscle layers, in any place, but they are most common in particular areas. In the area of the collarbone, they cause local pain and refer pain over the front of the shoulder. In the breastbone area, TrPs can broadcast intermittent, intense pain to the front of the chest and down the inner aspect of the arm. This can include a feeling of chest tightness, often mistaken for angina. These TrPs can radiate pain to the inside top of the forearm, as well as to the little finger side of the hand, including the last two or more fingers. If you find arrhythmias and no other sign of heart problems, check for TrPs. Chest pain that persists after a heart attack is frequently caused by these TrPs.
Pectoralis minor TrPs are located most often in an area about midway between the clavicle and nipple, and about midway between the edge of the breastbone and the outer edge of the upper arm. These TrPs send pain over the front of the chest and shoulder. Pain may run down the inner side of the arm and include the last 3 fingers. Pain from a left side pectoralis minor TrP can mimic angina. These TrPs can also entrap the axillary artery, as well as the brachial plexus nerve. The radial pulse may disappear as your patient moves the arm to different positions (Simons, Travell and Simons, 1999, p 851). When you relieve the TrP, the pulse is restored.
Many cases of Raynaud’s phenomenon have a TrP component. Numbness and odd sensations of the 4th and 5th fingers are common with these TrPs. There may be peculiar sensations over some parts of the forearm and over the palmar side of the first three and a half fingers. Paradoxical breathing perpetuates this TrP, as does poor posture. Check standing and sitting movements, and ask about sleep positions. Blood vessel entrapment by these TrPs does not produce the hand puffiness associated with scalene entrapment. Connective tissue TrPs in scar tissue of the attachment area in some rotator cuff tissues may cause referred tenderness, hot prickling pain, and lightning-like jabs to the pectoralis area.
Ensure that the bodyworkers to whom you refer patients have a firm knowledge of Travell and Simons’ Trigger Point Manuals. Repetitious exercises are contra- indicated in myofascial TrP therapy. You cannot strengthen a muscle that harbors a TrP. Many physical therapists do not understand this. Inappropriate therapy is a preventable perpetuating factor. Contraction of pectoralis muscles may pull down the SCM muscle group and work to perpetuate TrPs there. Forward rotated shoulders are a sign of this combination at work. If involved, the pectorals TrPs must be treated before the SCM TrPs can be successfully treated. Chest tightness may also be due to TrPs in the sternalis muscle.
Sternalis TrPs cause a deep ache under the breastbone, extending over the entire region of the breastbone and below. This can cover the upper chest and front of the shoulder on the same side, including the underarm and upper arm on the little finger side to the elbow. This produces an ache that feels like a heart attack or angina and is independent of body movement. Trigger points can occur anywhere within the sternalis, but they are often found in the upper two-thirds and to the left of center at mid-sternal level.
TrPs in the jaw and neck can contribute referred chest pain (Rusiecki 1998). Overburdening these muscles can cause TrPs. These TrPs can be formed during a heart attack or other visceral disease. When coronary artery disease and TrPs coexist, remember myofascial constriction from the TrPs can cause (treatable) further narrowing of the arteries. If your patient has angina or has had a heart attack, s/he probably has these TrPs, as these events can be initiating factors. Treating the TrPs may reduce the symptom level.
If these or any TrPs keep recurring, in spite of proper treatment, you must find the perpetuating factor. That could be a visceral problem, for example. Such organic disease can cause TrPs. Relieving the TrPs may relieve the symptoms for a short period of time, but the underlying problem will still be there.
Alvarez Lario B., J. L. Alonso Valdivieso, L. J. Alegre Lopez, S. C. Martel Soteres, J. L. Viejo Banuelos and A. Maranon Cabello. 1996. Fall in hemoglobin oxygenation in the arterial blood of fibromyalgia patients during sleep. Am J Med 101:54-60.
Bou-Holaigah, I., H. Calkins, J. A. Flynn, C. Tunin, H. C. Chang, J. S. Kan and P. C. Rowe. 1997. Provocation of hypotension and pain during upright tilt table testing in adults with fibromyalgia. Clin Exp Rheumatol 15(3):239-246.
Bradley LA, N. L. McKendree-Smith, G. S. Alarcon, L. R. Cianfrini. 2002 Is fibromyalgia a neurological disease? Curr Pain Headache Rep 6(2):106-14.
Caidahl, K., M. Lurie, B. Bake, G. Johansson, and H. Wetterqvist. 1989. Dyspnoea in chronic primary fibromyalgia. J Intern Med 226(4):265-270.
Clauw, D. J. 1995. Tilt table testing as a measure of dysautonomia in fibro- myalgia. J Musculoskel Pain 3(Suppl 1):10 (Abstract).
Cohen, H. L. Neumann, A. Alhosshle et al. 2001. Abnormal sympathovagal balance in men with fibromyalgia. J Rheumatol 28. 581-9.
Curtis, B. M., J. H. O’Keefe Jr. 2002. Autonomic tone as a cardiovascular risk factor: the dangers of chronic fight or flight. Mayo Clin Proc 77(11):45-54.
Martinez-Levin M. 2002. Management of dysautonomia in fibromyalgia. Rheum Dis Clin North Am 28(2):379-87.
Martinez-Lavin, M., M. Vidal, R. E. Barbosa et al. 2002. Norepinephrine-evoked paininfibromyalgia.Arandomizedpilotstudy[ISRCTN70707830]. BMC Musculoekel Disord 3(1):2.
Magaldi M., L. Moltoni, G. Biasi et al. 2000. Role of intercellular calcium ions in the physiopathology of fibromyalgia syndrome. Boll Soc Ital Biol Sper 76(1-2):1-4.
Neoh, C-A. 1995. Subjective shortness of breath and trigger points of levator scapular muscles. J Musculoskel Pain 3(Suppl 1):27 (Abstract).
Nilsson, P.M., A. Kandell-Collen, H. I. Andersson. 1997. Blood pressure and metabolic factors in relation to chronic pain. Blood Press 6(5):294-8.
Ogzocmen S., O. B. Cimen, O. Ardicoglu. 2002. Relationship between chest expansion and respiratory muscle strength in patients with primary fibromyalgia. Clin Rheumatol 21(1):19-22.
What Your Cardiologist Should Know About FMS and CMP
by Devin J. Starlanyl © 1995-1999 Page 5
Pellegrino, M. J., D. Van Fossen, C. Gordon, J. M. Ryan and G. W. Waylonis. 1989. Prevalence of mitral valve prolapse in fibromyalgia: a pilot investigation. Arch Phys Med Rehabil 70(7):541-543.
Raj, S. R. D. Brouillard, C. S. Simpson. 2002. Dysautonomia among patients with fibromyalgia: a noninvasive assessment. J Rheumatol 27(11):2660-5.
Simons D. G., J. G. Travell, and L. S. Simons. 1999. Travell and Simons' Myofascial Pain and Dysfunction: the Trigger Point Manual: Volume I, edition 2: The Upper Body. Baltimore: Williams and Wilkins
Weiss, D. J., T. Kreck and R. K. Albert. 1998. Dyspnea resulting from fibromyalgia. Chest 113(1):246-249.
|Posted on March 20, 2015 at 8:35 AM|
Interesting Article on overall cost of having images before utilizing PT
|Posted on December 31, 2014 at 9:15 PM|
Infraspinatus and its’ Trigger Points:
The Infraspinatus Muscle
Anatomy & Biomechanics: Let’s begin with a few brief anatomical and biomechanical details of this muscle. The infraspinatus muscle is found on the back of the shoulder blade and extends laterally to attach to the posterior aspect of the head of the humerus (upper arm) bone. This muscle has two important jobs:
Lateral Rotation of the Arm: Contraction of this muscle rotates the arm to the outside at the shoulder. The simple act of raising your hand to wave hello to someone is a good example of the infraspinatus muscle at work (among others).
Stabilize the Shoulder Joint: As one of the rotator cuff muscles, the infraspinatus contracts to stabilize the shoulder joint and keep the head of the humerus from slipping out of its socket during shoulder movement.
Syngeristic Muscles: The infraspinatus gets some help with its jobs from some of the other muscles in the shoulder girdle. The teres minor and deltoid (posterior head) muscles assist with lateral rotation of the arm, and the other rotator cuff muscles team up to assist with stabilizing the glenohumeral joint during various arm movements. The major antagonists to the infraspinatus are the subscapularis and pectoralis major muscles, both of which act to medially rotate the arm.
The Infraspinatus Trigger Points & Referred Pain
This muscle can contain three trigger points, arranged in a triangular pattern within the belly of the muscle. In my experience, the lower trigger point is the most common and most active in shoulder complaints. Referred pain from these trigger points is experienced deep in the front of the shoulder joint and along the upper arm. The pain may also spill down into the forearm and hand regions in severe cases.
Associated Trigger Points: Prolonged referred pain from these trigger points can activate the deltoid trigger points on the front of the shoulder. Referred pain in the forearm region may also activate wrist trigger points over time.
What Causes Infraspinatus Trigger Points?
Trigger points are activated (or reactivated) primarily by some form of muscular overload or trauma. In the infraspinatus muscle, overload can occur with any activity or event that requires a person to reach backwards with the arm or that keeps the arm raised to the front for long periods. Examples include:
throwing a baseball or football
forehand stroke in tennis
walking a large dog that pulls on the leash
long hours working at a computer keyboard with no elbow support
bracing for a fall or slip by reaching behind the body
long drives with the hands positioned on the top of the steering wheel
beginning a new resistance training (weight lifting) routine will often overload any of the rotator cuff muscles
Infraspinatus Symptoms & Disorders
Patients/clients with active trigger points in this muscle will present with the following symptoms:
Front of Shoulder Pain: This is the hallmark symptom for the infraspinatus trigger points. The pain often feels like it is deep within the shoulder joint, causing many clients to believe the shoulder joint itself is damaged.
Inability to Reach Behind the Back: Patients will report that they are unable to reach behind their back to fasten a bra or get their wallet out of a back pocket. These movements require significant internal rotation of the shoulder, which stretches the tense muscle and aggravates the trigger points within it.
Inability to Raise Arm Up To Head: Patients often report that they are unable to raise their arm up to wash their hair, brush their teeth, or even to bring food to their mouth while eating.
Inability to Push With Arms: Patients will complain of shoulder pain when using their arms to push up out of a chair or when pushing up out of bed in the morning. Weight lifting exercises like the bench press, inclined bench press, and military press are nearly impossible with active infraspinatus trigger points.
Shoulder Pain at Night: Infraspinatus trigger points can be a double-edged sword when trying to sleep on the side. If the client lays on the affected shoulder, the weight of the upper body can compress the trigger points and produce referred pain. If the client lays on the unaffected shoulder, the upper arm may hang down in front of the body and place the affected infraspinatus in a prolonged stretched state, aggravating the trigger points again. In severe cases, the client may be forced to sleep in a sitting position to prevent the pain from disturbing their sleep.
Bicipital Tendonitis: The role that infraspinatus trigger points play in many cases of bicipital tendonitis deserves special mention here. This condition is characterized by tenderness and pain in the biceps brachii (front) region of the upper arm, and is prevalent in baseball pitchers, football quarterbacks, and tennis players. I haven’t had very many cases of TRUE bicipital tendonitis in my personal practice, but every case that I have seen was easily resolved by deactivating the Infraspinatus trigger points.
Treatment of the Infraspinatus Trigger Points
It is important for the therapist to check for and address any trigger point activity in the supraspinatus and deltoid muscles after treatment of the infraspinatus trigger points. Deltoid trigger points are likely to form in response to the referred pain from infraspinatus trigger points, and supraspinatus trigger points are nearly always coconspirators in rotator cuff issues.
|Posted on December 6, 2014 at 12:45 AM|
Pectoralis Minor Trigger Points:
The pectoralis minor muscle is the little brother of the pectoralis major muscle. Like all little brothers, the pectoralis minor wants to do everything that big brother does, so it’s no surprise that trigger points in these two muscles have almost identical referred pain patterns.
These pain patterns start in the front of shoulder and can extend down the inside of the arm, elbow, forearm, palm of the hand, and into the pinky, ring, and middle fingers.
Not to be outdone by big brother, a tense pectoralis minor muscle can also entrap nerves in the armpit region that cause pain, numbness, and tingling to travel down the arm and into the hand.
The Pectoralis Minor Muscle
Location: The pectoralis minor is a small, thick muscle that lies in the chest region near the shoulder, underneath the larger pectoralis major muscle.
Function: This muscle functions to stabilize the shoulder girdle against the rib cage during downward thrusting movements of the arm, like when using crutches, chopping wood, or raising oneself out of a pool with your arms.
Muscle Attachments & Structure: The pectoralis minor originates on the coracoid process on the front of the scapula (shoulder blade) and splits into three sections that travel diagonally downward and medial to attach to the 3rd, 4th, and 5th ribs.
Muscle Actions: Contraction of the pectoralis muscle pulls the shoulder blade downward (depression) and forward (protraction) on the ribcage. Conversely, if the shoulder is held in place by the levator scapula and trapezius muscles, contraction of the pectoralis minor can elevate the upper ribcage and assist in inhalation.
Biomechanical Considerations: Chronic tension in the pectoralis minor can produce “winging of the scapula” in which the vertebral edge and lower tip of the scapula stick out from the rib cage and become visually prominent.
Tension in this muscle can also cause it to compress (entrap) the nerves of the brachial plexus in the shoulder region, producing neurogenic pain and numbness that is experienced in the forearm, hand, and fingers. It may also restrict blood flow to arm by compressing the axillary artery. Because of these entrapments, trigger point activity in this muscle can be a major contributor to thoracic outlet syndrome (along with scalene trigger points).
The Pectoralis Minor Trigger Point
Pectoralis Minor Muscle Pain
The diagram above shows the referred pain pattern associated with the primary trigger point. The pain concentrates in the anterior shoulder region, though it may also extend across the chest. It will also frequently travel down the inside the upper arm, elbow, forearm (on the pinky side). It can also occasionally refer to the palm, and into the pinky, ring and middle fingers.
This pain pattern is almost identical to that produced by the trigger points in the clavicular division of the pectoralis major.
Pectoralis Minor Symptoms & Disorders
Clients with an active pectoralis minor trigger point will present with any or all of the following symptoms or clinical findings:
Pain in the anterior shoulder region, extending into the chest region when severe.
Pain that travels down the inside of the arm to the pinky, ring, and middle fingers.
Like with the pectoralis major trigger points, if this pain is experienced in the left shoulder, chest, and arm, it can be confused with the pain from heart disease or a heart attack.
Pain on the inside aspect of the elbow, that mimics the pain of medial epicondylitis or “golfer’s elbow”
Numbness or tingling in the forearm, hand, and fingers, like that associated with carpal tunnel syndrome and/or thoracic outlet syndrome.
A weak or absent pulse at the wrist of the affected arm.
Difficulty in reaching forward and up with the affected arm.
A depressed shoulder girdle combined with winging of the scapula on the affected side.
What Causes Pectoralis Minor Trigger Points?
The following events or activities may activate or reactivate the pectoralis minor trigger points:
Trauma to the chest from a car accident
Whiplash from a car accident
Fracture or bruising of the upper ribs
Prolonged use of crutches
Hyperventilation or heavy breathing
Emotional or mental stress
Carrying a heavy backpack or purse over the shoulder
The head-forward, sunken-chest posture that is common in people that work at computers for long periods.
Previous or intermittent cardiac pain from a heart attack or angina pectoris.
Thoracic Outlet Syndrome
Medial Epicondylitis or “Golfer’s Elbow”
Carpal Tunnel Syndrome
Cervical Radiculopathy or herniated disk
Treatment of Pectoralis Minor Trigger Points
Important Note to the Reader: If you, or a client, is experiencing left sided shoulder and arm pain, it is imperative that a examination by a cardiologist be done immediately. Trigger point referred pain from the pectoralis muscles may occur secondarily to underlying heart disease, which must be ruled out or treated before trigger point therapy is indicated.
|Posted on November 23, 2014 at 8:40 PM|
External Oblique Abdominal Trigger points….Just in Time for Thanksgiving!!!!
If you are like me and LOVE food….then we both need to watch out eating this Thanksgiving not only for obvious reasons but that bloated feeling after stuffing ourselves with Turkey and dressing could activate trigger points in our abdominals which can lead to some nasty consequences.
The abdominal oblique muscles form the lateral wall of the abdomen and function to move the trunk relative to the pelvis. Contraction of these muscles, along with the other abdominal muscles, also acts to increase the pressure inside the abdominal cavity, which is necessary for the proper functioning of the abdominal organs.
The trigger points in these muscles are unique in that they primarily produce symptoms associated with abdominal organ dysfunction or disease. Many times, these abdominal trigger points are created by referred pain originated from the abdominal viscera, and will persist long after the visceral dysfunction has resolved itself.
Additionally, these trigger points often refer pain to the testicles and genitalia.
Because these muscles are prone to overload from emotional stress, core body mechanics, postural distortions, and visceral dysfunction (including eating quite a large Thanksgiving meal!), they are frequently a hotbed of trigger point activity.
The Abdominal Oblique Muscles
Location:The Abdominal Oblique muscle group forms the lateral abdominal wall. The two muscles in this group are the External Oblique and Internal Oblique, with the Internal Oblique lying deep to the External Oblique.
Function: The abdominal muscles (or core muscles) function to form the foundation for all gross movements of the body. Contraction of these muscles occurs in advanced of bodily movement to stabilize the spine in position and allow it to serve as a base for other muscles to act against. This stabilizing contraction flows from the inside out, beginning with the tranversus abdominis, followed by the internal oblique, external oblique, and finally the rectus abdominis.
The abdominal muscles also contract together to increase pressure, facilitating urination, bowel movements, vomiting, child birth, venous blood flow out of the abdomen, and forced exhalation.
Contracting together (both sides simultaneously) the abdominal oblique muscles produce forward flexion of the trunk (spine) on the pelvis.
Contracting unilaterally (on one side only) the external oblique acts to rotate the trunk towards the opposite side (moving the opposite shoulder backwards), while the internal oblique acts to rotate the trunk towards it (moving the opposite shoulder forward).
Contracting unilaterally, both muscles act to laterally flex the trunk (spine) to the same side.
The Abdominal Oblique Trigger Points
As shown in the diagram below , there are three potential trigger points in the abdominal oblique muscles:
Trigger points are often located in the lower outside quadrant of the abdomen near the Anterior Superior Iliac Spine (A.S.I.S) on the front aspect of the hip crest.
Another area that trigger points are found in the external oblique muscle that overlies the ribcage, a few inches below and lateral to the xyphoid process of the sternum (chest) bone.
Abdominal Muscle Pain
The diagram above also shows the referred pain patterns associated with the abdominal oblique trigger points.
The two lateral trigger points refer pain to the groin, testicles (and genitalia), and diagonally across the abdomen.
The upper trigger point refers pain in the upper abdomen and lower chest region, and produces symptoms similar to those of heartburn and hiatal hernia.
Abdominal Oblique Symptoms & Disorders
Clients with active oblique trigger points will present with any or all of the following symptoms or clinical findings:
Pain in the deep epigastric region, such as those symptoms associated with heartburn or hiatal hernia
Pain in the groin, testicles, bladder and lower abdominal region
Belching, stomach distention, diarrhea
What Causes Abdominal Trigger Points?
The following events or activities may activate or reactivate the oblique trigger points:
New abdominal exercise program
Punching or kicking from cardio kickboxing or martial arts class
Visceral disease such as peptic ulcer or intestinal parasite
Abdominal surgery scar
Constipation related straining
Prolonged sitting in a twisted position
Bloating or distention from overeating
|Posted on November 19, 2014 at 8:45 PM|
In 1972, Dr. Neer first introduced the concept of rotator cuff impingement to the literature, stating that it results from mechanical impingement of the rotator cuff tendon beneath the anteroinferior portion of the acromion, especially when the shoulder is placed in the forward-flexed and internally rotated position.
Neer describes the following 3 stages in the spectrum of rotator cuff impingement:Stage 1, commonly affecting patients younger than 25 years, is depicted by acute inflammation, edema, and hemorrhage in the rotator cuff. This stage usually is reversible with nonoperative treatment. Stage 2 usually affects patients aged 25-40 years, resulting as a continuum of stage 1. The rotator cuff tendon progresses to fibrosis and tendonitis, which commonly does not respond to conservative treatment and requires operative intervention. Stage 3 commonly affects patients older than 40 years.
As this condition progresses, it may lead to mechanical disruption of the rotator cuff tendon and to changes in the coracoacromial arch with arthritis along the anterior acromion. Surgical anterior acromioplasty and rotator cuff repair is commonly required. In all Neer stages, etiology is impingement of the rotator cuff tendons under the acromion and a rigid coracoacromial arch, eventually leading to degeneration and tearing of the rotator cuff tendon.
Although rotator cuff tears are more common in the older population, impingement and rotator cuff disease are frequently seen in the repetitive overhead athlete. The increased forces and repetitive overhead motions can cause attritional changes in the distal part of the rotator cuff tendon, which is at risk due to poor blood supply. Impingement syndrome and rotator cuff disease affect athletes at a younger age compared with the general population.
The shoulder consists of 2 bones (humerus, scapula), 2 joints (glenohumeral, acromioclavicular), and 2 articulations (scapulothoracic, acromiohumeral) that are joined by several interconnecting ligaments and layers of muscles. Minimal bony stability in the shoulder permits a wide range of motion (ROM). Soft tissue structures are the major glenohumeral stabilizers. Static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. Dynamic stabilizers include the rotator cuff muscles, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles (eg, pectoralis major, latissimus dorsi, serratus anterior). The rotator cuff consists of 4 muscles that control 3 basic motions, abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor muscles control external rotation, and the subscapularis muscle controls internal rotation. The rotator cuff muscles provide dynamic stabilization to the humeral head on the glenoid fossa, forming a force couple with the deltoid to allow elevation of the arm. This force couple is responsible for 45% of abduction strength and 90% of external rotation strength. The supraspinatus outlet is a space formed on the upper rim, humeral head, and glenoid by the acromion, coracoacromial arch, and acromioclavicular joint. This outlet accommodates passage and excursion of the supraspinatus tendon. Abnormalities (including trigger points situated within the muscle belly) of the supraspinatus outlet have been attributed as a cause of impingement syndrome.
Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described how variations in acromial size and shape can contribute to impingement. Cadaveric studies show 3 variations in acromion morphology, as follows: type 1 is flat, type 2 is curved, and type 3 is hooked anteriorly. Although the curved configuration was the most common (43% prevalence, compared to 17% flat and 40% hooked), the hooked configuration most strongly was associated with full-thickness rotator cuff tears. Other sites of impingement in the supraspinatus outlet space include the coracoacromial ligament (where thickening can occur) and the undersurface of the acromioclavicular joint (where osteophytes can form). The medial coracoid rarely is involved. These impingement sites in the supraspinatus outlet are compressed further when the humerus is placed in the forward-flexed and internally rotated position, forcing the greater tuberosity of the humerus into the undersurface of the acromion and coracoacromial arch. Nonoutlet impingement also can occur. Causes may be loss of normal humeral head depression from either a large rotator cuff tear or weakness in the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. This condition also may occur because of thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.
Overuse or repetitive microtrauma sustained in the overhead position may contribute to impingement and rotator cuff pathology. Shoulder pain and rotator cuff disease are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, volleyball, tennis). Secondary impingement often is attributed to impingement, which seldom is mechanical in nature in young athletes. Rotator cuff disease in this population may be related to subtle instability, and, therefore, may be secondary to such factors as eccentric overload, muscle imbalance, glenohumeral instability, or labral lesions. This has led to the concept of secondary impingement, which is defined as rotator cuff impingement that occurs secondary to a functional decrease in the supraspinatus outlet space due to underlying instability of the glenohumeral joint. Secondary impingement may be the most common cause in young athletes who frequently place large, repetitive overhead stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures, which leads to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendons. These increased demands may lead to rotator cuff pathology (eg, partial tearing, tendonitis). Furthermore, as the rotator cuff muscles fatigue trigger points develop which can contribute to prolonging the patients cycle of pain. This in turn can cause the humeral head to translate anteriorly and superiorly, impinging upon the coracoacromial arch. This leads to rotator cuff inflammation.
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In these patients, treatment should also address underlying instability as well as trigger point muscle dysfunction. The concept of glenoid impingement has been advanced as an explanation for partial-thickness tears in throwing athletes, particularly those involving the articular surface of the rotator cuff tendon. Such tears may occur in the presence of instability due to increased tensile stresses on the rotator cuff tendon from abnormal motion of the glenohumeral joint or increased forces on the rotator cuff necessary to stabilize the shoulder.
Arthroscopic studies of these patients note impingement between the posterior superior edge of the glenoid and the insertion of the rotator cuff tendon with the arm placed in the throwing position (abducted and externally rotated). Lesions were noted along the area of impingement at the posterior aspect of the glenoid labrum and articular surface of the rotator cuff. This concept is believed to occur most commonly in throwing athletes and must be considered when assessing for impingement.
|Posted on October 13, 2014 at 9:35 PM|
Lateral epicondylitis is commonly known as “tennis elbow.” This condition is essentially tendonitis in the outside part of the elbow. Tendonitis is inflammation of a tendon. A tendon is a group of cord like fibers which attach a muscle to a bone. Tendons can become irritated either thorough overuse or trauma. With lateral epicondylitis this is usually from returning to sporting activities to fast and too vigorously. However, it may occur from excessive overuse such as the constant use of a drill or screwdriver. Trauma can also cause tendonitis. If the elbow is hit or struck, "tennis elbow" or lateral epicondylitis may result. Trigger points can maintain the painful cycle of tendonitis long after the initial injury has healed. Trigger points adaptively shorten the muscle which continues to pull on the painful tendon which continues the inflammatory cycle.
Pain is the primary symptom. It will be located at the outside part of the elbow, either on the bone or in the muscle areas above and below that bony area. Pain usually begins slowly and increases over several weeks. The discomfort is commonly described as hot or burning and the areas may actually feel warm or be red. Swelling may also be present. Taut rope like bands may be present as well. In more severe cases, the pain may be present at all times and begin to expand away from the area of initial pain. If the tendonitis has not become excessive, pain may be felt only during use.
Activities that are problematic are usually associated with extending the wrist, turning the palm upward, or straightening the elbow. But in severe cases, any movement of the wrist and elbow may be difficult.
Treatment depends on the severity of the inflammation. Rest is a primary consideration. Since the tendon attaches directly to the muscle, use of the muscle places stress on the tendon, which will continue to irritate the tendon. A splint may be issued to temporarily immobilize the affected area and prevent use of the muscle. Your physician may prescribe anti-inflammatory medications.
Physical therapy treatment may include manual and manipulative therapy to the elbow joint, therapeutic modalities such as low level laser therapy, iontophoresis, ultrasound, electrical stimulation, heat, or ice. These are all meant to decrease pain and localized inflammation. There are also therapeutic exercises and stretches which may speed recovery. It is important to follow the guidelines for the rest and exercise, because tendonitis can become inflamed again very easily. If you have had multiple episodes of tendinitis in the same area over several years, you may find it takes longer to heal. Also, in some cases, a procedure known as friction massage may be utilized.
If symptoms persist for a long time, deep and superficial dry needling may be indicated. Consult us at Bluegrass Doctors of Physical Therapy, PLLC
|Posted on September 26, 2014 at 9:20 PM|
Ever feel that horrible stabbing pain underneath your knee cap (patella) whle trying to go up or even worse DOWN stairs? This may be a condition known as patellofemoral syndrome or chondromalacia patella. What the heck does that mean? Traditionally these are the diagnoses that describe a "fraying" of the cartilage on the back of the patella (knee cap). What causes this? While there are many debates on what causes this condition there are some general agreements. Certain anatomical variations in morphology( AKA the way we are born and put together) can cause the patella to track laterally to the outside of the groove it normally sits in. This coupled with weakness in certain quad and hip muscles then give rise to pain referral patterns that cause this pain to persist. These same muscles can also cause your knee to "lock up" or feel as though your knee may "give way" while walking or going down or up stairs.
How do we treat this you may ask? The Bluegrass Doctors of Physical Therapy, provide an innovative, comprehenisive treatment approach that involves the most effective manual therapy, taping, dry needling and strengthening techniques that can have your knee pain under control in as few as 2 visits!
To find out if that nagging knee pain you have been having is Chondromalacia Patella contact us today or book your initial evaluation online!
|Posted on September 19, 2014 at 1:00 PM|
A trigger point is a clinical name given to describe “hyperirritable spots in skeletal muscle that are associated with palpable nodules in taut bands of muscle fibers” (Travell, 1992). So in other words, a focal point within the tissue that is painful, and is most commonly described as a “knot” in the muscle. Now of course the tissue is not “tied in a knot”, but a skilled practioner will be able to feel and isolate this “mini-spasm” within the tissue.
Trigger points are significant because they alter the function of the muscle tissue. The muscle will be tighter, weaker, and create a pattern of pain that often refers to other areas. Have you ever had a headache from working at a computer too long? That could likely be the referred pain of a trigger point you feel, often in the neck or shoulders. Identifying the cause of a trigger point is probably the most significant clinical finding about it – that trigger points are not normal, and they will often point to an underlying cause such as poor posture, repetitive movement or strain, over-exertion, and sometimes the guarding response of a deeper underlying injury. Somatic (muscle) pain can be very debilitating and limiting, and a skilled practitioner will consider and test many factors when making an examination.
A common clinical technique to release a trigger point is through what is called an ischemic compression. An ischemic compression is when the therapist isolates the trigger point, and compresses it with pressure (often using a thumb to be precise). When compressed, the trigger point’s pain referral is often heightened temporarily, but quickly eases as the tissue releases. Ischemia means “a restriction in blood supply”, so by limiting blood supply to the trigger point through this compression technique, the muscle is deprived of essential nutrients (such as O2) needed to continue to contract and the result is that the tissue relaxes somewhat. This is an easy and effective way to help make trigger points smaller, as well as make an active trigger point reduce to a latent trigger point.
What is the difference between a latent trigger point and active one? Most commonly people refer to ACTIVE trigger points as ones that are ACTIVELY causing pain. I always educate my patients that active trigger points are ANGRY. These are the guys that are giving off constant pain referral and sending messages to the brain and spinal column that we are "hurt" or something is "wrong" within the tissue of the body. These can often mimic other pain referral patterns in the body, such as Sciatica, rotator cuff tears in the soulder and even pinched nerves in our neck.
Latent trigger points are Trigger points that have not become active yet however will give a pain referral pattern if you press on them. I often teach my patients that latent trigger points are LAZY. They cause dysfunction in the muscle unit because they don't want the muscle they are in to do any work. Essentially they take up space and gripe some if you move a certain way or try to use them in specific muscle unit. These trigger points need to be released in addition to active trigger points because often times these will develop into active trigger points if allowed to be left alone and contue contrubuting to muscle dynfunction.
The most common method that the doctors at Bluegrass Doctors of Physcial Therapy use to inactivate trigger points and COMPLETELY release them is through Superficial and/or deep dry needling.