Pathologie du genou

Les affections du genou sont en augmentation croissante dans la population. Cette augmentation est due aux traumatismes sportifs et à la prévalence croissante d'arthrose du genou liée au vieillissement de la population. La prise en charge multidisciplinaire dans la phase aiguë mais surtout chronique de ces affections paraît primordiale pour en réduire la morbidité. En juin 2001, s'est tenu le symposium «Pathologie du genou», sponsorisé par Pharmacia-Pfizer. Son but était de faire la lumière sur les dernières nouveautés en thérapeutique dans ce domaine et de synthétiser la prise en charge de ces pathologies sous l'angle de la chirurgie orthopédique, de la rhumatologie et de la médecine physique. Il était animé par les professeurs T.L. Vischer (Division de rhumatologie, HUG), J. Garcia (Département de radiologie, HUG), D. Fritschy (Policlinique de chirurgie, HUG), ainsi que les docteurs P.-A. Guerne (Division de rhumatologie, HUG) et J.-L. Ziltener (Clinique romande de réadaptation, Sion).

Sémiologie et traitement chirurgical

(Pr D. Fritschy)

L'accident récent

En Suisse, les sports les plus souvent impliqués dans les pathologies du genou sont le ski et le football.

Une seule question prime : s'agit-il d'une entorse grave ? Concernant les symptômes, les éléments de gravité sont : un craquement lors de l'accident, l'impression de genou flottant, l'apparition rapide d'un épanchement et une limitation lors de l'extension. Cliniquement, la mobilité active d'abord puis passive est testée, les points douloureux sont recherchés (insertions ligamentaires et tendineuses, interligne articulaire, rotule). Puis, il faut tester la stabilité du genou avec le test de Lachman, genou presque en extension (positif si lésion du ligament croisé antérieur). Un effacement de la tubérosité tibiale antérieure en flexion du genou signe une lésion du ligament croisé postérieur. On recherche également une laxité des ligaments latéraux, et une lésion méniscale (déficit d'extension si interposition due à une anse de seau ou une languette, test de Mac Murray, grinding test, etc.).

En cas d'épanchement, celui-ci doit être ponctionné stérilement. La présence d'une hémarthrose signe une effraction osseuse dans 5% des cas surtout en présence de lobules graisseux (fracture chondrale ou ostéochondrale, arrachement ligamentaire), une déchirure ligamentaire dans 80% des cas (presque toujours le ligament croisé antérieur) ou une déchirure méniscale dans 15% (présence de vaisseaux dans sa périphérie). Les lésions combinées sont possibles. L'évolution d'une hémarthrose traumatique non traitée est défavorable dans 80% des cas1 et un épanchement doit donc toujours être investigué.

Diagnostics possibles :

I Entorse bénigne, qui est une contusion ou une distorsion simple sans atteinte ligamentaire ou méniscale.

I Entorse grave avec lésion ligamentaire, et/ou déchirure méniscale, et/ou fracture.

I Fractures : luxation de la rotule avec arrachements de fragments, arrachement ligamentaire (souvent chez l'enfant et l'adulte jeune avec arrachement de l'attache au plateau tibial), torsion-collision épine-condyle, fracture de Segond (avulsion de la capsule avec fragments arrachés sur le condyle externe et sur le tibia). A relever que les fractures chondrales (fragment cartilagineux) ne se voient pas sur les radiographies standards et que l'IRM est alors l'examen de choix.

I Lésions tendineuses (quadriceps, rotulien), lésions vasculaires ou nerveuses lors de luxation surtout, lésions des parties molles, des bourses, etc.

Le bilan complémentaire comprend des radiographies de face, de profil et en axial de la rotule, pour exclure une fracture et préciser le cadre osseux, et éventuellement une IRM. Le traitement chirurgical n'étant pas urgent, il faut d'abord immobiliser le membre inférieur par une attelle, prescrire des cannes et des antalgiques, puis débuter rapidement les exercices de remusculation du quadriceps, la fonte musculaire commençant dès le traumatisme initial.

Le genou chronique post- traumatique

Le potentiel de cicatrisation du ligament croisé antérieur (LCA) est médiocre, et une laxité ligamentaire sur une déchirure ancienne du LCA, avec douleurs, lâchages et blocages, va retentir sur les autres structures du genou, surtout les ménisques puis le cartilage, menant à une arthrose post-traumatique.

Le traitement peut se faire par chirurgie arthroscopique avec résection à minima des lésions méniscales, régularisation des lésions cartilagineuses et chirurgie ligamentaire par greffe autologue avec un autre tendon (rarement : allogreffe). Une plastie de reconstruction est indiquée principalement chez les patients actifs entre 15 et 35 ans, gênés dans leurs activités quotidiennes ou chez les sportifs professionnels. Avant l'âge de 15 ans, il faut attendre que la croissance soit bien avancée pour éviter de léser le cartilage de croissance.

La méniscectomie classique par arthrotomie est arthrogène et aujourd'hui, le ménisque doit être préservé dans la mesure du possible. L'arthroscopie est indiquée uniquement pour une intervention chirurgicale et non pour poser un diagnostic, qui se fait par IRM.

Après méniscectomie, les principaux facteurs arthrogènes sont le volume de ménisque excisé, la qualité du cartilage restant, la présence d'une laxité ligamentaire, le morphotype (surcharge pondérale, défaut d'axes). Les dégâts peuvent être prévenus par une modification des activités, le renforcement musculaire, le port d'une orthèse et une éventuelle reconstruction ligamentaire.

Le genou arthrosique post-traumatique

Les symptômes sont : douleur, tuméfaction, diminution de mobilité et instabilité.

Traitement chirurgical :

I L'arthroscopie permet une toilette articulaire avec excision de tissu méniscal dégénératif, une régularisation des lésions cartilagineuses et éventuellement une résection des ostéophytes.

I L'amélioration est transitoire, de quelques mois à quelques années.

I La correction des défauts d'axe par ostéotomie a pour but de stabiliser l'évolution de l'arthrose avec en moyenne sept ans d'effet bénéfique.

I L'arthroplastie partielle ou totale, qui est un resurfaçage partiel ou complet des zones arthrosiques, est devenue très fréquente avec 265 000 patients qui en ont bénéficié aux Etats-Unis et 6000 en Suisse.

Le point de vue du rhumatologue

(P.-A. Guerne)

Lors d'une monoarthrite, l'épanchement doit toujours être ponctionné (technique de ponction : cf site Internet : www.rheuma-net.ch) pour compter le nombre de cellules (pathologie non inflammatoire si cellules 1,4).

Monoarthrites infectieuses

L'origine de ces arthrites peut être pyogène (diagnostic par la culture), neisserienne (culture souvent négative, diagnostic par frottis et PCR dans les urines), sur maladie de Lyme (culture non sensible, diagnostic par Elisa et Western Blot), à Brucella (diagnostic par sérologie), dans le cadre d'une maladie de Whipple (arthrite à caractère palindromique, avec troubles digestifs et malabsorption, diagnostic par biopsie jéjunale et PCR), à mycobactéries (faire des biopsies si les cultures sont négatives).

Arthrites microcristallines

Goutte

Si l'acide urique sérique est supérieur à 420 mmol/l, le diagnostic de goutte a une sensibilité de 90%, mais une spécificité de 54% seulement. Donc celui-ci se fait par la mise en évidence de cristaux dans le liquide synovial (sensibilité : 84%, spécificité : 99%). De plus, il faut rechercher la présence de tophus et d'érosions sur les radiographies.

Le traitement d'attaque reste classique : AINS, stéroïdes en injection intra-articulaire ou i.m., ou per os 30-50 mg/j pendant sept à dix jours, éventuellement colchicine. Concernant le traitement prophylactique, les indications à l'introduction d'un hypo-uricémiant comme l'allopurinol (avec ajustement de la dose selon la créatinine) sont : plus de trois crises/an, une néphropathie uratique, des tophus, des signes radiologiques. Ils doivent être introduits à distance, c'est-à-dire plus de deux semaines après la dernière crise, sous couvert d'un traitement prophylactique (AINS à petites doses, colchicine 0,5-1 mg/j).

Chondrocalcinose

L'arthrite aiguë à pyrophosphate de calcium est le plus souvent spontanément résolutive. Les radiographies étant peu sensibles et peu spécifiques, le diagnostic se fait également par la mise en évidence de cristaux dans le liquide de ponction. Si nécessaire, le traitement de la crise est le même que celui de la goutte. Il est utile de rechercher une pathologie associée : hémochromatose, hyperparathyroïdie, hypomagnésémie sévère. Il existe aussi une arthropathie chronique qui peut être mono-, oligo- ou polyarticulaire, et qui se traite soit par des AINS, de la colchicine à petites doses, ou des stéroïdes à faibles doses.

Dans le diagnostic différentiel d'une mono-arthrite du genou, il faut aussi évoquer une spondylarthropathie, une arthrite réactionnelle (à streptocoques, à chlamydia, etc.), une hémochromatose. Une polyarthrite rhumatoïde a rarement un début mono-articulaire.

Pathologies non arthritiques

Les plus fréquentes sont l'arthrose, la nécrose aseptique, les fractures lentes, les bursites prépatellaire ou infrapatellaire d'origine microtraumatique, infectieuse ou inflammatoire. Le diagnostic de ces dernières se fait par ponction avec compte cellulaire et culture.

Traitement médicamenteux de l'arthrose

I Le traitement classique comprend les analgésiques non opiacés, les AINS, les injections intra-articulaires de stéroïdes, les opiacés si nécessaire.

I Une viscosupplémentation avec des chondroprotecteurs en injection intra-articulaire (Synvisc®, Osténil®, etc.) montre une efficacité supérieure au placebo sur les douleurs (à 6 mois : 50% des patients sont satisfaits) et comparable aux AINS sans les effets secondaires. La réponse est plus favorable dans les stades initiaux de l'arthrose, et moins favorable s'il y a un épanchement. Pour l'instant, il n'y a pas beaucoup d'évidence sur l'effet protecteur du cartilage (ralentissement de destruction).

I L'effet du sulfate de chondroïtine (Condrosulf®, Structum®) est principalement antalgique.

I La glucosamine, non vendue en Suisse, aurait des résultats positifs selon une étude récente.2 Vu les nombreux biais de ce travail, d'autres études sont nécessaires avant de conclure définitivement à un effet thérapeutique de ce produit.

I La synoviorthèse est utile si l'épanchement est récidivant et répond partiellement aux injections intra-articulaires de stéroïdes.

Examens radiologiques en fonction de la sémiologie

(Pr J. Garcia)

Les critères essentiels d'un bon examen radiologique sont le choix adéquat de la technique, qui doit être la plus sensible et la plus spécifique selon la durée des symptômes, la rigueur dans l'analyse et l'interprétation des images ainsi que la prise en compte de la corrélation radio-clinique.

I Lors de traumatisme, les radiographies sont indispensables, de face, de profil et axiale. Si la clinique est suspecte et les premières radiographies normales, des obliques sont nécessaires. Selon la gravité du traumatisme, un CT-scan doit être effectué. L'IRM permet la découverte de lésions non visibles sur les radiographies : œdème, lésions ligamentaires ou méniscales. De bonnes coupes IRM permettront de mettre en évidence des signes indirects de rupture du LCA. En cas de déchirure méniscale, les lésions visibles à l'IRM vont jusqu'à la surface du ménisque. Chez les jeunes, il existe déjà des petites hétérogénéités qui sont des dégénérescences mucoïdes et donc banales.

I En cas d'arthrose fémoro-tibiale, les radiographies sont à demander en position debout pour bien apprécier l'espace articulaire, en extension et en flexion à 30° afin de mieux déceler l'arthrose débutante.

I L'arthrose fémoro-patellaire se met en évidence avec des radiographies axiales à 30° pour analyser la partie inférieure de la rotule, à 60° pour la partie moyenne et à 90° pour la partie supérieure. Un mauvais positionnement du malade peut mimer un pincement articulaire (erreur technique).

I L'IRM avec injection de produit de contraste est la meilleure technique pour diagnostiquer une chondromalacie.

I L'échographie reste l'examen de choix lors de pathologies tendineuse, ligamentaire et périarticulaire (kystes, bursites, etc.)

I Les pathologies inflammatoires sont investiguées par l'IRM.

I L'IRM est positive dès les premiers jours en cas d'algodystrophie, avec un œdème qui régresse dans les deux mois, et un épanchement (diagnostic différentiel : fracture par insuffisance).

I Lors de nécrose aseptique, l'IRM est positive dès les premiers jours avec un œdème non spécifique puis des images caractéristiques dans les trois premiers mois.

I La ponction est le premier geste à effectuer en cas de suspicion d'arthrite septique.

L'imagerie est utile pour le bilan des complications.

I Les pathologies tumorales sont bien visibles sur les radiographies standards. Le bilan d'extension de la lésion dans l'os et les tissus mous se fait par IRM.

Place de la médecine physique

(Dr J.-L. Ziltener)

Troubles dégénératifs

Les effets des traitements physiques passifs (cryothérapie, thermothérapie, TENS, ondes courtes) sont positifs uniquement dans les stades aigus. La physiothérapie manuelle peut améliorer la mobilité mais doit toujours être associée à des exercices à domicile.

Il existe une corrélation entre le gain de force et la diminution des douleurs après un minimum de huit semaines d'exercices globaux et en série de renforcement musculaire. Une diminution de l'efficacité est néanmoins notée à long terme. Les exercices aérobiques tels que la marche et/ou le vélo, trois fois par semaine pendant trois mois, améliorent la fonction, la qualité de vie et les douleurs.

Syndrome fémoropatellaire

Lors d'atteinte de la surface cartilagineuse ou de troubles de la dynamique rotulienne (dysplasie, instabilité, etc.), le traitement consiste à rétablir la balance musculaire entre le muscle vaste interne et le vaste externe, associé à des exercices d'étirements des muscles tenseurs de fascia lata et ischiojambiers. L'efficacité d'un taping rotulien est controversée mais un effet subjectif antalgique est toutefois souvent noté. Lorsque le taping a un effet antalgique mais est mal supporté, une orthèse peut être prescrite.

Lésions récentes du LCA

Comme l'a mentionné précédemment le professeur Fritschy, le traitement chirurgical n'est pas urgent. L'immobilisation doit être courte, entre 2-6 semaines. Le traitement fonctionnel pur avec reprogrammation musculaire et exercices de proprioception a pour objectif d'éviter l'instabilité. Il doit être débuté précocement pour éviter l'atrophie musculaire et les adhérences périrotuliennes, d'abord par électrostimulation si nécessaire puis par renforcement musculaire. Il y a peu de différence entre le traitement conservateur et le traitement chirurgical sur la fonction à long terme, mais la chirurgie apporte une meilleure stabilité de l'articulation.

Bibliographie :

1 Mariani PP, Puddu G, Ferretti A. Hemarthrosis treated by aspiration and casting. How to condemn the knee. Am J Sports Med 1982 ; 10 : 343-5.

2 Reginster JY, Deroisy R, Rovati LC, et al. Long term effects of glucosamine sulphate on osteoarthritis progression. Lancet 2001 ; 357 : 251-6.

A Conservative Approach to the Management of Anserina Bursitis

By R. Vincent Davis, DC, PT, DNBPM

The pes anserinsa bursa is located on the medial aspect of the tibia situated deep to the tendons of the sartorius, gracilis, and the semitendinosus and is superficial to the insertion of the tibial collateral ligament at the tibial tubercle. 
The function of this bursa is the same as elsewhere in the body components. It reduces friction between surfaces.

Although it is commonly not palpable clinically, in the event of inflammation, the examiner may be able to detect effusion and thickening due to synovial irritation. The bursal synovium is subject to pathological change due to trauma, infection, metabolic disease, occupational strains, and neoplasms. Of course, this writing is dedicated to those aspects of treatment which relate to physiatry.

Acute direct trauma typically results in distention of the bursal sac with synovial effusion and may appear as a local swelling. Although this swelling may resolve spontaneously, from a therapeutic perspective, resolution may be enhanced by a compression wrap and rest. Initially, cryotherapy may reduce the intensity of the swelling and, after 3-4 days, heat packs may enhance the absorption of localized edema. One percent hydrocortisone pulsed phonophoresis @ 0.5 W/cm2 X 5 minutes, t.i.d., p.r.n. for pain and/or swelling may be administered.

In chronic traumatic bursitis, where the bursal wall becomes thickened and fibrotic with small accumulations of fibrin within the synovial cavity, synovectomy is commonly required, after which a compress is applied and a new bursa then forms.

Acute and chronic infectious bursitis is treated with appropriate antibiotic therapy. The area of the genicular region overlying this bursa may appear reddened, be markedly warm to palpation, with muscle spasm limiting local joint ROM. There may be fever, neutrophilia, and an elevated ESR. These clinical features usually resolve with continued use of the appropriate antibiotics.

Gouty bursitis involves urate deposits in the bursal wall with symptoms comparable to the infectious signs/symptoms. Biopsy, microscopy, and sometimes radiographic imaging reveal the effects of urate crystals interstitially. Although contrast therapy may provide for some initial relief, any treatment must be accompanied by antigout therapy in the form of purine restriction, increase in dietary vegetables, and possibly colchicine derivatives per oral.

There is no specific, effective, physiatric treatment for malignant lesions of the bursae. These lesions would be referred to other specialties for appropriate care.

Although seldom observed at this site, calcific bursitis may be considered a by-product of recurrent lesions of a sprain/strain/trauma character. Since this process favors the Glimcher hypothesis, it is capable of shifting from a soluble to an insoluble state and back again based on the chemical modification of the interstitial fluids. It is therefore possible to modify this calcific lesion to a noncalcific state with appropriate treatment. Acetic acid phonophoresis (three percent) may be effective, but care must be exercised in its application to avoid tissue irritation due to the effects of hydrogen ion concentration. Ultrasonic energy is applied with the lesion submerged in a one percent or two percent acetic acid solution (vinegar is three percent to four percent) @ 0.5 to 0.75 W/cm2 X 7 minutes. Any complaint of discomfort by the patient, for any reason, should result in immediate discontinuation of treatment and rinsing of the submerged tissue. There is some question as to the efficacy of this treatment.

Although the foregoing therapeutic regimen is commonly effective, in the event of continued complaints and/or objective findings, referral for orthopedic consultation is recommended.

References

Davis RV. Therapeutic Modalities for the Clinical Health Sciences, 2nd ed., 1989, Library of Congress Card TXU 389-661.

Griffin and Karselis. Physical Agents for Physical Therapists, 2nd ed., Thomas Publishers, 1982.

Krupp and Chatton. Current Medical Diagnosis and Treatment, Lange Publications, 1980.

Turek. Orthopedics -- Principles and Their Application, 3rd ed, Lippincott.

DISH and Stenosis

By Deborah Pate, DC, DACBR

Diffuse idiopathic skeletal hyperostosis (DISH) is a degenerative disorder of unknown etiology that frequently occurs in patients over 60. The distinguishing characteristic of this disorder is the presence of excessive ligamentous calcification and ossification of ligaments in the spine and extraspinal locations (Figure 1). 
For those of you who graduated when I did or before, this disorder was often inaccurately called Forrestier's disease. It was initially thought this disorder may be a type of ankylosing spondylitis (AS) which it is not, and the two should not be confused as their etiologies are entirely different.

DISH has strict diagnostic criteria which distinguishes it from degenerative disc and joint disease and ankylosing spondylitis. The following criteria have been established: 1) flowing calcifications and ossifications along the anterolateral aspect of at least four contiguous vertebral bodies with or without osteophytes; 2) preservation of disc height in the involved areas and an absence of excessive disc disease; 3) absence of bony ankylosis of facet joints and absence of sacroiliac erosion, sclerosis, or bony fusion, however narrowing and sclerosis of facet joints are acceptable.

DISH occurs most commonly in the thoracic spine (97% of cases). It presents as laminated calcification and ossification along the anterolateral aspect of the vertebral bodies, continuing across the intervertebral disc spaces, which are relatively preserved. Ossification may extend to involve both the right and left lateral aspects of the vertebral column, but is more common and exuberant on the right side, presumably due to the inhibiting effect on ossification by a left sided, pulsating descending thoracic aorta.

Lumbar spine abnormalities in DISH are almost as frequent as thoracic spine abnormalities. Lumbar spine changes include hyperostosis along the anterior aspect of the vertebral bodies. With progression, cloud-like increased bone density and pointed body excrescences develop. Additional findings that can occur are close apposition of spinous processes or ossification of interspinous ligaments, mild to moderate disc space narrowing, and apophyseal joint space narrowing and sclerosis. Due to the ossification of the calcification and ossification of ligaments which can include the joint capsule, foraminal and central stenosis can occur at any spinal level.

In the cervical spine, bony prominence may become so extensive that a thick bony plate is formed anteriorly and may cause dysphagia. Alterations can occur on the posterior aspect of vertebral bodies, most often in the cervical spine. These radiographic features include osteosclerosis of the posterior vertebral margin, posterior vertebral osteophytosis, and calcification or ossification of the posterior longitudinal ligament. Cervical myelopathy and cord compression has been associated with patients demonstrating bony proliferation along the posterior aspect of the vertebral bodies.

Extraspinal manifestations of DISH are not uncommon and may even be present in absence of significant spinal changes. These extraspinal changes consist of hyperostosis at sites of tendon and ligament attachment to bone, para-articular osteophytes, and ligament ossification. Generally in the peripheral skeleton, periosteal spurs arising at the site of osseous attachment of the tendon are more prominent than true calcification of the tendon itself. These ossifications extend into the fibers of the tendon, particularly the Achilles' tendon and plantar aponeurosis, triceps, and quadriceps tendons.

In my experience a majority of patients with DISH have clinical symptoms which include: stiffness, restricted motion, and tendinitis. The discomfort is intermittent and nonradiating, stiffness occurs most often in the morning upon arising and dissipates within an hour of mild activity. The discomfort can return in the late evening and become aggravated by sitting or cold, wet weather. These complaints are initially apparent in the thoracolumbar spine. Several years after the initial onset of symptoms, stiffness and pain can progress to involve other areas of the spine, including the extremities. The disorder can progress to the point of causing significant neurologic involvement, however the radiographic changes should also indicate probable stenosis. These patients generally respond well to chiropractic treatment, (with the exception of patients with significant spinal stenosis), but they require care on a continuing basis due to the chronicity of the symptoms.

Other diseases can also be present along with DISH, we are allowed unfortunately, to have more than one disorder at a time. The most common disorders are spondylosis deformans and rheumatoid arthritis.

Movement of the Nervous System

By Warren Hammer, MS, DC, DABCO

Doctors treating peripheral entrapment lesions with myofascial techniques, such as friction massage, active release and other fascial release methods, implicitly accept the concept of movement of the nervous system.

According to Butler,¹ "The nervous system must have optimal mechanical function just like the other structures in the body." If we think of both the central and peripheral nervous system as a continuous tissue tract, our concepts relating to evaluation and treatment of the human condition will reach new dimensions.

In the central nervous system in spinal flexion the posterior columns move more than the tracts on the anterior side of the neuraxis; the opposite occurs with spinal extension. In lateral bending the tracts will be stretched more on the convex side. The spinal canal is 5cm-9cm longer in flexion than extension.² During elbow flexion the ulnar nerve stretches while the median and radial nerves shorten. The reverse occurs with elbow extension. McLellan and Swash³ placed needles in the median nerves of volunteers and found that wrist and finger extension pulled the nerve down an average of 7.4mm. Elbow flexion caused 4.3 mm of upward movement. Local treatment of neural adhesions in these areas might make use of this information. The sympathetic trunk located just anterior to the cost-transverse joints must also have the ability to move. Lateral thoracic spinal bending stretches the contralateral side while cervical extension stretches the cervical sympathetic trunk and ganglia.⁴ Cervical flexion may tense the sympathetic plexus near the carotid and vertebral arteries. It is absolutely necessary for nerves to be able to move within the connective tissue that surrounds it, and within itself for normal function. Peripheral nerves can be limited to connective tissue just adjacent to the nerves, as well as intraneural limitation not allowing sliding and elongation. Leahey's Active Release technique has proven extremely successful in restoring movement to the peripheral nervous system.

In a slumped position where a patient sits at the edge of a table with the knees flexed at the edge, the examiner has the patient flex the spine (not the hips). The patient then bends the neck (chin to chest), and the examiner applies an added pressure to the head and shoulders. The patient is then asked to extend a leg and dorsiflex the foot. Bilateral leg extension and foot dorsiflexion should be compared. In this case a patient might feel pain in the right hamstring. If the patient holds the right leg in extension and brings only his flexed head back into extension there could be a significant decrease in right hamstring pain. This reaction may be considered neurogenic in origin, demonstrating the continuum of the nervous system. If there was bilateral thigh pain in leg extension during the slump test and a decrease of pain on head extension, this might be considered a normal reaction.¹ The slump test, among many other things, demonstrates that the continuous tissue tract of our nervous system can limit combinations of motion. Nerve tension testing can be used to examine this continuum for pain and limitation at local areas. It is possible to use nerve tension stretching as a treatment. For example, a Slump Test procedure can at times be used to treat a sciatica by having the patient actively stretch the sciatic nerve by maintaining a slumped sitting position, legs extended, neck flexed just up to the point of pain and then switch to an upright sitting position with the leg flexed and the neck an shoulders in neutral or extension. Just holding the extended leg for about 10 seconds at a time without creating a severe increase in pain may help to release the sciatic nerve.

References 

1. Butler DS. Mobilisation of the Nervous System. New York, Churchill Livingstone, 1991. 
2. Breig A. Adverse Mechanical Tension in the Central Nervous System.Almqvist & Wiksell, Stockholm: 1978. 
3. McLellan DL, Swash M. Longitudinal sliding of the median nerve during movements of the upper limb. J of Nuerology, Neurosurgery and Psychiatry. 39:566-570;1976. In: Butler DS. Mobilisation of the Nervous System. New York, Churchill Livingstone, 1991. 
4. Schneider RD, Schemm GW. Vertebral artery insufficiency in acute and chronic spinal trauma with special reference to the syndrome of acute central cervical spinal injury. J of Neurosurgery. 18:348-360:1961. In: Butler DS. Mobilisation of the Nervous System. New Y

Meralgia Paraesthetica

By Moses Sweis

Meralgia paraesthetica, also known as lateral femoral cutaneous nerve entrapment, is a condition that afflicts many females. It produces pain of the dysesthesia type. The area affected becomes very sensitive to even light touch. 
The patient gets a sensation of burning, tingling at an area that is localized to the anterior lateral thigh, between the inguinal ligament and the knee. The pain is usually triggered by prolonged standing or sleeping in a particular position, and relieved by change in position. There is no motor involvement, therefore there is no muscle atrophy or reflex change.

The lateral femoral cutaneous nerve is formed from the L2, L3 nerve roots. It exists under the inguinal ligament and supplies the sensory component of the skin at the anterior, lateral, and posterior areas of the thigh. This nerve can be compromised under the inguinal ligament by obesity, trauma, pregnancy, tight clothing or a tight belt. Also, Evans' Illustrated Essentials in Orthopedic Physical Assessmentstates that "Like other entrapment neuropathies, lateral femoral cutaneous nerve entrapment is apt to occur with metabolic disorders, which may make the peripheral nerves vulnerable to pressure."

Another complication to this condition is its ease to be misdiagnosed as a L2/L3 nerve root compression syndrome. With nerve root involvement, you would also have motor dysfunction, which is not present with this condition.

To illustrate this, let's take an actual case I worked with just a few months ago. A 30 year old, 133-pound female of 64 inches in height presents to my office complaining of pain in her left thigh. She describes the pain as a numbness, pins and needles sensation that burns upon touch. This has been present for over six years and localized to the distal 1/3, anterior/lateral surface of the left thigh. A worse position for the patient is lying on her left side with the knee flexed. Physical, neurological, and orthopedic testing revealed no abnormalities, other than abnormal dysesthesia at the area mentioned above. What complicates the etiology even more is that the patient is not obese, not pregnant, doesn't wear tight clothing and, overall, is healthy. She states that her previous chiropractor had treated her low back for over 10 visits with no progress. As a matter of fact, her condition got worse after the last few visits. Obviously, from her case history, I came to the conclusion that her previous DC had misdiagnosed her condition as a nerve root compression syndrome, not meralgia paraesthetica which my examination revealed.

Knowing the low success rate of treatment for this condition, I explained the prognosis to the patient and began treatment. The treatment involved ultrasound over the inguinal ligament, muscle stretching of the anterior and lateral thigh and chiropractic adjustments to the spine. After a few treatments, deep tissue massage was implemented. She was also given vitamin B6 as nutritional support. The patient showed some progress with some days no dysesthesia felt. But unfortunately, towards the end of her treatment plan, her condition regressed to its normal stage.

If any doctor knows of a treatment other than what was presented here and is successful for treating this condition, your input would be appreciated by me, my colleagues, and most certainly the patient.

References 

• Evans RC. Illustrated Essentials in Orthopedic Physical Assessment. St. Louis: Mosby, 1994 (pg. 322).
• Agur AMR. Grant's Atlas of Anatomy. Baltimore: Williams and Wilkins, 1991: 138, 164, 263.
• Van De Graff KM, Fox SI. Concepts of Human Anatomy and Physiology. Dubuque: Web, 1986: 494.

Exercise and Pregnancy

By Kim Christensen, DC, DACRB, CCSP, CSCS

Both exercise and pregnancy exert stresses on the body, and the cumulative effects must be considered when recommending a rehabilitative exercise program to pregnant women.¹Credible human research about the topic is sparse, and animal studies provide conflicting findings.

Chronic disorders such as diabetes, hypertension, and heart disease are clear reasons to discourage persons at risk from intense rehabilitative exercising while pregnant. Also, small or underweight women probably should be cautioned, since these women bear more premature and low birth weight infants than larger, normal-weight women.

Getting in Shape

Weight loss endeavors during pregnancy should be discouraged regardless of whether a decreased caloric intake or exercise is used, because neuropsychological abnormalities in infants have been associated with pregnancy. Adolescents are particularly prone to exercise during pregnancy, but a "get-in-shape" program should be deferred until after delivery if it is not undertaken before pregnancy. The existing level of aerobic fitness is an important factor in determining the eligibility of a pregnant woman for a rehabilitative exercise program. The effects of aerobic training are rapidly lost when activity ceases.

Walking is an excellent activity for the pregnant woman. Jogging should be discouraged, at least in the later stages of pregnancy, because of progressive lordosis and possible strain on the pelvic ligaments. A conservative approach to exercise seems wise because of its effects on the fetal heart rate and breathing movements. The maternal heart rate should not exceed 140 to 150 beats per minute for about 15 minutes, three to five times a week. Exercise at this level elicits an aerobic training effect in most women of childbearing age, while producing minimal fetal responses.

Gentle stretching and a warmup period before each exercise period are important measures. A cool down period of 10 to 15 minutes is also recommended. And because increased weight shifts anteriorly over the course of a pregnancy, it is also recommended that pregnant patients be fitted for custom made flexible orthotics. The ideal orthotic would be one which absorbs heel-strike shock, provides firm arch support and combats the high stress levels which commonly affect the lumbar spine of the mother-to-be.

Sedentary women should not begin vigorous rehabilitative exercise or try to get into shape during pregnancy. The time to get into good physical condition is before or after pregnancy. Once pregnant, a sedentary woman can begin a walking program or something similar. However, a woman who has been exercising can pursue a rehabilitative exercise program during pregnancy by adjusting the intensity of the program, according to how she feels, and keeping her heart rate in the 140 to 150 beats per minute range.

Fetal Heart Rates

Doppler monitoring of fetal heart rates, showing fetal bradycardia during vigorous maternal exercise, has given rise to concern for fetal safety. Because Doppler measurement of fetal heart rate during maternal exertion is difficult, two-dimensional ultrasonic imaging was used by Carpenter et al.² to record the fetal heart rate and determine the effect of submaximal and maximal maternal exertion and the incidence of fetal bradycardia.

Forty-five women with a mean gestation of 25 weeks performed exercise twice on separate days using a cycle ergometer. Resting measurements were taken with the women seated on the ergometer for 10 minutes. They underwent 85 submaximal and 79 maximal cycle ergometer tests.

Fetal cardiac activity was monitored continuously and videotaped during exercise and rest periods using a linear array two-dimensional ultrasound system. The average fetal heart rate did not change during maternal exertion, but 15 of 16 post-exercise episodes of bradycardia occurred within three minutes after maximal maternal exertion. There were 18 episodes of fetal bradycardia; one occurred during exercise.

Brief submaximal exercise up to 70% of maximal aerobic power seems to have no effect on fetal heart rate. Maximal exertion, on the other hand, is commonly followed by fetal bradycardia. The significance of this bradycardia is as yet unknown, but it seems prudent to recommend that pregnant women limit vigorous exercise to activities of no more than 150 beats per minute and conclude their exertion with a cool-down period.

Supine Exercise

Several investigators have monitored fetal hart rate (FHR) as a way to assess fetal hypoxia or distress in response to maternal exercise. An early study reported little effect on FHR, whereas later studies yielded conflicting results when using the FHR response to exercise as a screening test for uteroplacental insufficiency. Recent studies have reported a transient increase in baseline FHR. The effect of brief periods of mild, supine exercise on FHR in the late second trimester and mid-third trimester was studied by Nesler et al.³

Twenty-five healthy, regularly-exercising women were studied: 12 in the late second trimester, and 13 in mid third trimester. Although significant increases in maternal mean arterial pressure and pulse occurred, the exercise intensity was mild, with the average percent maximal pulse being 46 +/- 5% in the second trimester group and 49 +/- 5% in the third trimester group. Small increases in FHR were observed in both groups, which were insignificant statistically and physiologically. No patient experienced significant FHR abnormalities as a consequence of the exercise sequence.

These results indicate that pregnant women may continue submaximal supine exercise of short duration through the 36th week of gestation without harmful effects to the fetus. Thus, moderate exercising by pregnant women does not cause increases in the FHR. However, exercising while in a supine position instead of on a cycle ergometer may be a better choice. However, it appears from comparison of studies that the more vigorous exercise program used by Carpenter et al.² demonstrated no more danger to the fetus than did the more conservative program described by Nesler et al.³

Aerobic Exercise

The health and fitness of pregnant women at the onset of gestation affect the course and outcome of the pregnancy. Whether pregnancy reduces physical fitness as measured by maximal oxygen consumption between the second and third trimesters, and whether maintaining a regular exercise program during the second half of pregnancy influences fitness, were determined in 23 women by South-Paul et al.⁴ at the beginning of the second trimester.

Patients were randomly assigned to either a non-exercising or an exercising group. They completed a maximal progressive exercise test on a cycle ergometer at 20 weeks and 30 weeks, during which time pulmonary parameters or aerobic capacity were assessed.

The exercising women had greater improvement in aerobic capacity than the non-exercising women, manifested by increases in tidal volume and oxygen consumption and a stable ventilatory equivalent for oxygen. Pregnancy did not decrease the maximal oxygen consumption between the second and third trimesters, during which detraining could have been substantial.

This study points out the value of exercising during pregnancy. In fact, none of the women in this study was previously trained and the average baseline oxygen consumption was in the low range for both groups. Yet, when placed in a supervised exercise program, the exercise group improved their fitness, as demonstrated by an increased maximal oxygen consumption per kilogram of body weight.

The effects of exercise on the fetus are important in view of the increasing participation by women in rehabilitative exercise clinics. Dale et al.⁵ undertook a retrospective study of 21 women who had been pregnant in the past five years and who had participated in running during the course of pregnancy. A prospective sample of 12 women who were currently pregnant and running was also done with 11 controls matched with the runners for age, race, and parity. Electronic fetal monitoring was carried out in four subjects, all with favorable obstetric outcomes.

Subjects in the retrospective sample had a mean age of 30 years and had run for an average of four years; the mean prepregnancy weekly distance was 18.7 miles. Mean distances run in the three trimesters were 14.2, 10.9, and 6.6 miles a week, respectively. Eight of the 21 subjects competed in races while pregnant. Mean maternal weight gain was 24.4 pounds. In the prospective study, the only major obstetric complication in a runner was threatened abortion. There were no neonatal complications in the running group except for jaundice in an infant. Electronic fetal monitoring during treadmill running showed transient bradycardia, with a return of fetal heart rate to normal during continued exercise.

The course of pregnancy and complications appear to be similar in women who run during pregnancy and those who do not. Women who run exhibit a trend toward failure to progress during labor, resulting in an increased rate of cesarean section delivery. There is no evidence from Dale et al.⁵ of a compromised neonatal status in cases of women who run during pregnancy. Exercise appears not to seriously compromise uteroplacental function. Whether the fetal bradycardia observed during initial exercise is a response to transient hypoxia, a result of shunting of blood to the leg muscles, or an effect of other stress remains to be determined.

In the Dale⁵ study that evaluates 33 pregnant runners and 11 pregnant nonrunners, there is a more concerned note, perhaps, about potential major obstetrical complications in runners than controls, and the possibility of a higher Cesarean section rate in this group because of failure of progression during labor. More data would be necessary to confirm this, but this would be another argument for caution in prescribing running during pregnancy. There was no significant difference between runners and nonrunners with respect to weight gain, length of labor, and delivery, and the absolute incidence of obstetric complications. Dale5 did note fetal bradycardia, usually transient for a 2 1/2 to 3 1/2 minute interval, with spontaneous recovery during exercise. This is the point of concern. Again, pregnant women should limit exercise to activities requiring heart rates of no more than 150 beats per minute and conclude their exertion with a cool-down period.

References 

1. Snyder DK, Carruth BR. J Adolesc Health Care 1984; 5:34-36.
2. Carpenter MW, Sady SP et al. JAMA 1988; 259:3006-3009.
3. Nesler DL, Hassett SL, Brooke J. Am J Perinatol 1988; 5:159-163.
4. South-Paul JE, Rajagopo KR, Tenholder MF. Obstet Gynecol 1988; 71:175-179.
5. Dale E, Mullinax KM, Bryan DJ. Can J Appl Sports Sci 1982; 7:98-103.