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.
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.
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.
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.
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
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