PART XXI:

PHYSICAL THERAPIES AND

ADITIONAL METHODS

 

 

Although we suffer a chemically induced damage, and there is no known cure for it, some supportive physical therapies have been proposed by different people. Like with everything else, no consistent results have been recorded, and all therapies have shown beneficial effects for some, nothing for others, and unwanted consequences for the rest.

 

But not all are so controversial, and certain physical therapies are mandatory for given conditions, like for instance myofascial release for entrapments of nerves within the fascia layers of the muscles.

 

In this chapter we list some of the most debated therapies, without describing them in detail. For some of them we venture an opinion but it is only you, as always, who has to get all the information, and professional medical help, before starting any program or before rejecting any avaliable treatment.

 

 

149. MASSAGE

 

As said, there are no magic silver bullet treatments and no total agreement about how to treat pains and disabilities. Test the ones that help you most in maintaining your fitness, sanity and well-being. If you were very athletic prior to the floxing, your drama will probably multiply, because all your physical activities will come to an abrupt end for many years. Probably some of the following will help:

 

*      MECHANICAL: ultrasound; massage, especially deep massage and with the aid of steel tools by a specialized practitioner; stretching. They help with the regeneration, realignment of scar tissue and removal of by-products of the reactions. Releasing of the trigger points (entrapment of nerves in muscle bundles) that neurological deficits cause also can bring some temporary relief. Aggressive stretching of limbs affected with neuritis exacerbates neurological pains, and for some 18 hours or so, throbbing stabbing pains can be felt.

*      SUPPORTIVE: acupuncture; relaxation, meditation, occasional dry saunas, homeopathy, mesotherapy, gentle yoga. Hyperbaric oxygen can be of help for the first stages of acute musculoskeletal collapses, when people become bedridden.

*      EXERCISE: Especially controversial. For some it is positive only after you feel you are getting out of the acute phase: biking and swimming are preferred. Strengthening, especially isometric exercises, and several sports and exercises, should be introduced progressively. Somehow there is scattered evidence that excessive exercise can induce new relapses, which needs future clarification.

Later on in the report, see the section devoted to athletes.

 

 

150. STRENGTHENING AND STRETCHING

 

Is a critical part of any recovery program. They have to be adapted to the specific needs of the areas of the body that are treated. It is not covered in this version of the Flox Report. Most tendon deficits and nerve pains are much increased by weak muscles (due to neuromuscular junction injury), so the need for muscle strength becomes critical.

 

 

151. PHYSIOTHERAPY

 

If the reaction has been strong and the floxed person has many physical limitations as a consequence of the floxing, physical therapy by a good technician, can be of great help. The following case explains the professional approach to a possibly mild case of achilles tendinitis.

 

PHYSICAL THERAPIST MANAGEMENT OF FLUOROQUINOLONE-INDUCED ACHILLES TENDINOPATHY. Brenda L Greene

Probably you can find the whole article at this address:

http://www.ptjournal.org/cgi/content/full/82/12/1224

../..This case report described a patient whose Achilles tendinopathy was an adverse side effect of short-term antibiotic use. It illustrates the importance of awareness of relationships between adverse drug effects and musculoskeletal conditions. This case report also describes a patient's recovery from fluoroquinolone-induced tendinopathy. Decreased load-bearing ability of the tendon suggests that the first phase of rehabilitation should be a protective one. During the first month of rehabilitation with his first physical therapist, this patient's tendon was not protected and his symptoms worsened. Later, the heel lifts, counterforce bracing, and crutch use were all intervention strategies designed to decrease the tensile load transmitted to the Achilles tendon during walking. Although little is known about connective tissue healing subsequent to drug-induced toxicity, the literature does provide insight into connective tissue mutability and response to mechanical stress, in general. Too great a load results in microfailure and potentially macrofailure of the connective tissue, but lack of loading results in connective tissue atrophy and weakness. For this reason, it was necessary to find a balance between loading and unloading the tendon and to progressively stress the tendon over time in an attempt to increase the tendon's ability to tolerate greater stresses. The progressive exercise program was designed to gradually load the Achilles tendon in a controlled fashion. During the first 6 weeks, the patient was able to tolerate minimal progression of the exercise program, but during the last 5 weeks, his ability to resist loading increased weekly.

../...By understanding the nature of connective tissue remodeling, the intervention was designed to first protect the tendon and then to progressively load the tendon. During the initial 6 weeks of protection, however, when the tendon was structurally and mechanically altered from the toxic effects of the fluoroquinolone antibiotic, the progression was slow in comparison with the relatively faster initial recovery from acute overuse injuries that I have observed. The patient's improvement was nonlinear in that he made little progress in the first 7 weeks and made rapid progress in the last 4 weeks. In fluoroquinolone-induced tendinopathy, the tendon has the potential to rupture even after the cessation of medication usage.6 Adequate protection of the healing tendon, which lasts until the tendon regains its tension-bearing capacity, probably is important. The time frame for this patient's recovery was consistent with the range stated in Pattern 4D of the Guide to Physical Therapist Practice—2 weeks to 6 months and 3 to 36 visits. His entire recovery process took 5.5 months and a total of 24 physical therapy visits. He had 10 visits with his first physical therapist and 14 visits with me.

Case reports are a good approach to describe relatively infrequent pathologies, such as Achilles tendinopathy secondary to fluoroquinolone antibiotic use. However, due to the lack of controls in case reports, the experiences with this patient may not be generalizable to other patients and the patient's recovery could have resulted from factors other than the physical therapy intervention.

 

 

152. MYOFASCIAL RELEASE

 

It is not a massage technique properly speaking, If you have suffered a floxing with big musculoskeletal involvement and keep on attempting to exercise vigorously, you are a firm candidate to develop almost intractable trigger points (bundles of muscles, fascia and nerves) if as a consequence of the floxing:

*      you have some atrophy, or lack of strength and have problems to increase your muscular mass.

*      you have some stiffness and muscle pain specially after exercise (fascia degradation).

*      you are lean and fibrous in nature.

 

Floxed persons develop multiple trigger points, specially if they exercise to be active physically. The trigger poinst develop thanks to two mechanisms:

 

A. Local injury to tissues causes tearing in the fibers of muscle, tendon, ligaments, and tissue lining the bone called periosteum. These injuries are caused because muscles have lost part of their strength due to defects at the neuromuscular junction, because connective tissues, specially fascias are degraded and cause stiffness, and because the muscle cells are not served properly due to the degradation of vessels and extracellular matrix. Such tears do not heal due to continuing stress and impaired healing caused by the toxicity of quinolones.

 

B.Systemic toxicity (accumulation of toxins in all tissues) that creates painful tender points in areas of chronic mechanical stress, such as the back of upper neck, shoulders, lower back, knees, buttocks, legs, and other tissues. Systemic toxicity also causes the formation in the blood of micro-curdles which clog tiny vessels and further impede blood flow and healing.

 

In many patients these trigger-points (muscles) contain highly palpable ropy cords and are prone to suffer from pain referred from trigger points in the matrix of these cords. The cords behave not as muscle, but as dense fibrotic tissue. The pain referred from trigger points in these cords can best be stopped with ultrasound or negative galvanism. But the relief is brief unless the muscles are stretched what some times is difficult or impossible. So, cross-friction technique with hooks is used to stretch and loosen these muscles (cord bundles).

Your trigger points can develop anywhere, but we are to mention only some common ones that are located at the upper buttocks area, specially in the gluteus minimus muscles. Trigger points in these muscles frequently result in well-defined patterns of pain referral that may be variously experienced as “sciatica” pain. This pain can be intolerably persistent and excruciatingly severe. The trigger point source of the pain is deep in the gluteal musculature and almost all of the pain becomes apparent in a remote structure along the leg.

 

Figure 31 depicted by a therapist that has been treating floxed persons for seven years, based on a drawing by Myosymmetries International Inc.. Red knots are the locations of

fig. 31

 
typical trigger points, and blue areas are the zones where the pain is felt.

 

An exercise that can help to strengthen the gluteus minimus is to stand on one leg on a Boheler's plate because the primary function of the gluteus minimus is as an abductor (opening the leg) of the thigh, helping to keep the pelvis level during single-limb weight-bearing.

 

As common as gluteus minimus trigger points in floxed persons are lower back, piriformis and abdominal trigger points.

 

The treatment for these trigger points is myofascial release, using blunted steel hooks. A severely floxed person may need this therapy for many years.

 

If your fascias have become degraded by the floxing, it is possible that they also get stuck at some points. If muscles do not move freely with respect to each other, or if a nerve passes through the area where the fascia is not doing its job, it will be compressed, or stretched, or irritated and then very high pains will develop all along the length of the nerve. 

 

CASE REPORT (Real example). One floxed person developed cipro-induced neurotoxicity of the crural nerve (main nerve of the leg), that was also reflected in the conductivity tests. As a result, his quads and hamstrings atrophied and the ileotibial band (tight and narrow muscle band that runs along the outer side of the leg from the hip to the knee) got overloaded. The fascia between quads and ileotibial band was in bad shape too due to the floxing, as many other fascia layers of his body, with a lot of adhesions, scar tissue formation and deposition of abnormal material. The femoral cutaneous nerve passes through that fascia, and it got altered causing very high pains along the buttock, outer side of the leg, outer side of the knee and proximal (upper) tibiais muscle end. These pains still last after 5 years and are constant at times, causing a limp, preventing the victim from sleeping and causing much misery. The victim only gets some temporary relief when he takes a deep fascia release at the layer between ileotibial band and quads.  Take into account that the deep fascia of the leg forms a complete investment to the muscles, and is fused with the periosteum (sheath of bones) over the subcutaneous surfaces of the bones. It is continuous above with the fascia lata (ileotibial band), and is attached around the knee to the patella, the ligamentum patellæ, the tuberosity and condyles of the tibia, and the head of the tibula. Behind, it forms the popliteal fascia, covering in the popliteal fossa; here it is strengthened by transverse fibers, and perforated by the small saphenous vein. It receives an expansion from the tendon of the Biceps femoris laterally, and from the tendons of the Sartorius, Gracilis, Semitendinosus, and Semimembranosus medially; in front, it blends with the periosteum covering the subcutaneous surface of the tibia, and with that covering the head and malleolus of the fibula; below, it is continuous with the transverse crural and laciniate ligaments. It is thick and dense in the upper and anterior part of the leg, and gives attachment, by its deep surface, to the Tibialis anterior and Extensor digitorum longus; but thinner behind, where it covers the Gastrocnemius and Soleus. It gives off from its deep surface, on the lateral side of the leg, two strong intermuscular septa, the anterior and posterior peroneal septa, which enclose the Peronæi longus and brevis, and separate them from the muscles of the anterior and posterior crural regions, and several more slender processes which enclose the individual muscles in each region. A broad transverse intermuscular septum, called the deep transverse fascia of the leg, intervenes between the superficial and deep posterior crural muscles.

 

The following information has been adapted from a document of Myosymmetries International Inc. Myofascial Release (Muscle-Fascia-Release) is used for recovery from all types of physical injuries such as sporting injuries, back and neck pain, whiplash, stress-related muscular tension and repetitive strain injuries. Myofascial Release is also used in the treatment of immune system dysfunctions such as Fibromyalgia, Chronic Fatigue Syndrome, and others, and is mandatory in floxed persons with the symptoms and conditions listed above.


As you know by now, fascia is specially targeted by the toxicity of quinolones. Fascia is the most pervasive tissue in the body, surrounding and enveloping everything from whole muscle groups and bones down to individual cells, including individual muscle fibres, tendons, ligaments, nerves, viscera and the circulatory system in all its guises. Through the meninges and the dural tube fascia plays an enormous role in the central nervous system. Superficial fascia is attached to the underside of the skin, much like a body stocking and is the outer layer of a three-dimensional continous network which compartmentalises the body separating and surrounding each part. Fascia is entirely continuous throughout the body, therefore, if there is restriction in any part it will affect  other parts, sometimes at a distant point from the origin.


Each muscle fibre has a fascial binding, and so muscle and fascia are functionally linked, giving rise to the term 'myofascia' (muscle - fascia). Injuries or imbalances in the muscular system will be reflected in the fascia, and it is often restrictions in fascia which give rise to 'muscle' pain. Releasing fascia provides lubrication for the movement between muscle fibres and other structures. Circulatory and lymphatic vessels and nerves move through the body in fascial membranes providing feedback to the central nervous system. If fascia is not moving freely all other structures will experience painful restriction in movement. This phenomenon is behind those stiffness and soreness caused by physical activity in floxed persons.


Fascia is composed mainly of collagen (40%) and lubricating ground substance. Both muscle with its fascial sheaths and ground substance are 70% water - fascia acts like a sponge. With physical and emotional trauma it dehydrates - water is pushed out - rendering it hard and gel-like, thus reducing the lubricant qualities of the ground substance between the collagen fibres and decreasing the distance between the fibres. This leads to the collagen fibres shortening, thickening, and sticking together. Fascia which is shortened and hard compresses capilleries and nerves, causing pain, imbalance and discomfort, and resulting in decreased cardiovascular flow which further compromises healing capability. Myofascial Release brings about an increase of hydration of the ground substance, the collagen fibres and the whole of the fascial system. It increases the distance between the collagen fibres, allowing for further hydration and a decrease in compression around other structures.

 

It follows then that myofascial restrictions play a large part in pain syndromes. Fascia which is restricted can be extremely painful itself and cause surrounding fascia to stiffen protectively. Structures around restricted fascia cannot move without friction, compounding the problem. Continuous overload of an area can then lead to total fascial restriction in which movement is almost impossible without extreme pain. This will not show up in any orthodox medical tests, neither need the muscles themselves be directly involved or responsible. The pain resulting from myofascial restriction is often described as deep, sharp, dull, burning, diffuse, heavy, or 'like toothache'. Often it is difficult to pinpoint the exact location of the centre of pain and very often, if the cause is not treated and wider areas of fascia become affected, the pain can become generalized. Pain in the myofascial system is often referred pain, that is, the origin is in a seemingly unrelated, unaffected area. A myofascial practitioner will seek to treat the problem where it arises rather than where the symptoms emerge.


Myofascial Release is the term referring to a collection of techniques for separating layers of fascia, releasing restrictions, restoring elasticity, conductivity and hydration. A Myofascial Release practitioner will use a variety of techniques including gross or 'cross-hand' stretches, focused stretches, skin rolling, 'windmill' or J-stretches, fascial glide, deep 3-dimensional stretches, following fascia layers in their direction of ease, pulls, focused rebounding, shaking or rocking, tender point treatment and trigger point release. Other muscle release techniques may well be used during the same session and tendons, ligaments, muscle tissue and fascia will all be treated where necessary, either concurrently or separately.

 
Myofascial restrictions can lead to muscle imbalances as individual muscles and whole muscle groups are prevented from functioning fully because of myofascial pain, resulting in some becoming short and tight and others long and tight or atrophied. Weakness will occur in any case. It is therefore important to reestablish muscle balance when myofascial release has taken place. A specifically devised Pilates exercise programme, focusing on maintaining biomechanical balance and myofascial release, is excellent for reeducating the brain in correct muscle recruitment for each movement or postural hold.

 

QUINOLONE INDUCED MYOTENDINOPATHY

Vasuki Narayanasamy M.D, Harsha Vyas M.D, Guha Krishnaswamy M.D.

The Fluoroquinolones is a popular class of antibiotics due to its wide spectrum of activity, favorable pharmokokinetics and relative lack of side effects. They act by inhibiting DNA gyrase and topoisomerase IV resulting in ineffective bacterial DNA synthesis. Myotendinopathy is a major concerning side effect associated with the use of Fluoroquinolones. We are reporting cases of sartorius muscle and achilles tendon ruptures secondary to the use of quinolones.

Case report #1: This is an 82 year old female patient who presented to the clinic with left lower extremity pain and swelling after being treated for bronchitis with levofloxacin in her prior visit. On examination, the calf and dorsum of the left foot was associated with moderate swelling and ecchymosis around the insertion of Achilles tendon. Full range of motion at the ankle was limited due to pain. The pulses were intact. A MRI was performed since a tendon rupture was suspected due to the acute nature of presentation and a history of fluroquinolone use. The MRI showed a near full thickness of the Achilles tendon around 3 cm proximal to the calcaneal insertion. Patient chose the non surgical approach and was treated by non weight bearing cast.

Case report #2: This is a 72 year old male who presented to the clinic with  ecchymosis of right lower extremity and intense edema. He was treated with Gatifloxacin 10 days prior to this presentation for COPD exacerbation. Deep vein thrombosis was ruled out by Doppler U/S of the Lower Extremity. Further investigation by MRI showed rupture of the right Sartorius tendon at the insertion to knee. This is the first case to be reported for Gatifloxacin induced tendon rupture. He was treated initially by phonopheresis and continued conservative non surgical management since he was not a surgical candidate.

Conclusion: FQ induced myotendinopathy  has been reported extensively in the literature since the 80’s, due to the concern associated with the widespread use of  antibiotics in modern medicine. It has been associat