cranial osteopathy for infants, children and adolescents - a practical handbook ( sergueef )

6/1/2018 Cranial Osteopathy for Infants, Children and Adolescents - A Practical Handb...

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An imprint of Elsevier Limited

2007, Elsevier Limited. All rights reserved.

The right of Nicette Sergueef to be identified as author of this work has been asserted by her in accordancewith the Copyright, Designs and Patents Act 1988.

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First published 2007

ISBN-13: 978-0-443-10352-0ISBN-10: 0-443-10352-6

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responsibility of the treating practitioner, relying on independent expertise and knowledge of the patient,to determine the best treatment and method of application for the patient.

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CONTENTSCHAPTER. 1 THE BIRTH PROCESS AND THE NEW BORN,

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CHAPTU, DYSFUNCTIONS , 79D - ., _ _ ,.~ - - __ ..' ' ..... 10-pl, ,,,,,, -- - ~ ........ dru _

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CHAPTER 6 TREATMENT OF THE PATIENT, 117T' m' .. .



CHAPTeR 7

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............."""- "._01 ..... '_, I ~Owu ~ ' d' .. ' ' ' ' ' ' ' , , . , . , . . , . , . . , . , . . '..... ...,......-,~ o l .... ' ~ I f,(>r , , _ ~ -- . 61)O.pit '*' . ns '". . . . . .. ol . . . t.,f - - l,'''''''v, : 01 .... ) 1 0 ' 0 1 < _ 161- : .d '_'O)s..: . ol ' ............. ,(.45is considered patho-logic. Congenital kyphotic deformities are infre-quent and can be caused by a failure of formation of

the vertebral body or a failure of segmentation, forwhich the treatment is surgical.107 In the infant,tumor of the spine is also a potential cause of kypho-sis that requires specific medical attention.

In the juvenile period, Scheuermanns disease isa cause of kyphosis resulting from an alteration ofthe vertebral development. Wedging of the verte-bral bodies, the posterior height being greater thanthe anterior height, produces the kyphotic defor-mity. Boys are more frequently affected and theresultant back pain might be the trigger for an X-ray

where the diagnosis is made. Irregularities in theendplates of the vertebrae can be observed, particularly at the level of the lower thoracic and upperlumbar spine. Scheuermanns disease may also beassociated with scoliosis.108

Because kyphosis is a spinal deformity, it shouldnot be confused with poor posture. When examiningan infant who is seated without support, it is normato find a kyphosis of the thoracic and lumbar spineProprioception and muscular tone develop with ageto maintain adequate sagittal balance. Sagittal spinacurves change as a child grows.109,110The thoracickyphosis is more pronounced in males,111at a meanage of 12.8 years.112

More often, the exaggerated kyphotic curve isassociated with dysfunctional posture. Juvenileand adolescent kyphosis can be the result of poorposture, as a compensatory pattern to an extensiondysfunction elsewhere. Anterior displacement othe occipital bone on the superior articular surfaceof the atlas will project the chin forward, and theensuing postural compensation will result in anincreased thoracic kyphosis. This pattern is com-monly found in individuals who demonstrate orabreathing.

When encountered in a child, an apparentkyphosis may also be the result of protractionof the pectoral girdle. In this case, the thoraciccurve is not fixed in the kyphotic position andspinal backward bending can be achieved ondemand, although lack of flexibility is common. The

child is usually shy, and an extensioninternal rotation pattern may be present, either at the level ofthe pelvis or at the level of the SBS, the temporaor occipital bones. A thoracoabdominal diaphrag-matic dysfunction is very often associated withdiminished thoracic flexibility and reduced vitacapacity. The areas of the diaphragmatic attachments onto the inferior portion of the sternum andadjacent ribs might be the causative dysfunctionalagents.

An increased thoracic kyphotic curve is usuallycompensated for by an increase in the lumbar

lordosis. Kyphosis and lumbar lordosis generallycompensate each other. A correlation betweenthese two spinal curves has been found in most agegroups.113

The cervical and lumbar regions are normallylordotic. Hyperlordosis is an increase of the lumbarlordosis and is considered pathologic. It can beassociated with other conditions, such as develop-mental dysplasia of the hip or neuromuscular disor-ders. There may be a family history of hyperlordosisbut it can also follow trauma, commonly from


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196 CRANIAL OSTEOPATHY FOR INFANTS, CHILDREN AND ADOLESCENTS

athletic activities, particularly highly competitivesports, during periods of growth. Adolescents mayalso present with hyperlordosis as a consequenceof a developmental spondylolisthesis. With this dis-order, studies have shown an increase of hyperlor-dosis and sacral inclination, but a decrease of thoracickyphosis.114

The degree of lumbar lordosis is correlatedwith sacral position. Sacral anatomic extension(craniosacral flexion) is normally associated withdecreased lordosis; sacral anatomic flexion (cranio-sacral extension) is associated with increased lordo-sis. The global amplitude of the vertebral curves,cervical lordosis, thoracic kyphosis and lumbar lor-dosis changes with growth, but the association withthe position of the sacrum is constant under normalconditions.

The relationship between the cranial and thepelvic bowls, through the core link, is a fundamentalprinciple within the cranial concept. Cranial flexionis associated with sacral craniosacral flexion, andcranial extension is associated with sacral craniosa-cral extension. The vertebral anteroposterior curvesare decreased when flexion of the cranial base ispresent; conversely, there is an increase of the lor-dotic or kyphotic curves with extension of thecranial base.115

Physical examination and treatment

Early detection of kyphotic and lordotic curves is

important for successful treatment. The child shouldbe considered from a total body approach and theposture of the whole body should be evaluated in thestanding position:

Observe the pattern of weight-bearingmechanics.

Observe the feet for a pattern of inversion oreversion. A pattern toward eversion of the feet,and eventually flat feet, is consistent withincreased sagittal curves and cranial extensioninternal rotation.

Observe the knees. Genu valgum is consistent

with increased sagittal curves and cranialextensioninternal rotation.

Observe the pelvis for an increase of anteriortilt, with the sacrum in craniosacral extension.

Observe for pelvic asymmetry and anydifference in the greater trochanter andinnominate crest heights.

Observe the spine for an increase of theanteriorposterior curves. A pattern involvingall of the curves might be the consequence of

a cranial or sacral dysfunction with extensionand internal rotation. A pattern of increasedcurvature limited to a portion of the spinemay be associated with a dysfunction withinthe curve, in an adjacent spinal curve oradjacent junctions between the spinal APcurves.

Observe the pectoral girdle for protraction oran associated asymmetric pattern. A differencein shoulder heights is common. This suggestssomatic dysfunction in the thoracic spine withassociated sidebending and rotationalcomponents.

Observe the position of the head in relationof the rest of the body, in both the frontaland the sagittal plane. Forward displacementof the head is often associated with somaticdysfunction of the craniocervical or upperthoracic vertebrae.

Next, observe the child while they are moving.If necessary, have the child demonstrate activeflexionextension, sidebending and rotation of thespine to confirm previous observations. Muscles mayshow a difference in tension between anterior andposterior groups. Hyperlordotic children will presentwith increased tension in the hamstrings and hipflexors, while at the same time their abdominalmuscles will lack tension.

Tests of listening are performed on the innomi-nates, the sacrum, the lumbar and cervical vertebrae

and the cranium. The treatment of any identifieddysfunctional areas should follow using indirectprinciples. The postural response to effective manip-ulation is almost immediate. You should be able tosee improvement in the posture of the child after thefirst treatment.

Simple exercises may be recommended, particu-larly if poor posture is present. Pelvic tilt is useful,as are stretching the hamstrings and proprioceptiveexercises to increase body posture awareness. Thechild should be encouraged to judiciously practiceathletic activities, such as swimming and tai chi,

which will strengthen and balance the core musclesand improve flexibility and coordination.

Advice should be given that appropriatelyaddresses daily living conditions. For example, thepatient should avoid carrying a backpack on oneshoulder; rather, they should carry it using bothshoulders. They should avoid reading and writing ona flat horizontal surface and should work instead ona surface that is tilted approximately 20 to limitcervicothoracic flexion.



CLINICAL CONDITIONS 197CLINICAL CONDITIONS

Once the problem has been effectively addressed,the child may then be treated as needed, but theyshould be followed on a regular basis, at least annu-ally, until they have stopped growing.

PECTUS EXCAVATUM ANDCARINATUM

Pectus excavatum is a deformity of the anterior tho-racic cage in which the sternum is depressed in aconcave shape, whereas in pectus carinatum thesternum is protruded in a convex shape. Thesedeformities may or may not be associated withgenetic disorders or with scolioses. Decreased tho-racic cage compliance and reduced vital capacitymay be present, although the heart and lungs developnormally. Pectus excavatum and pectus carinatumare present at birth, but the parents usually do notbecome aware of the deformity until it becomesmore apparent with growth. Severe cases often resultin significant psychological impact, usually in earlyadolescence.

Pectus excavatum is frequently associated with anSBS extension pattern. This results in internal rota-tion of the paired structures, specifically the pectoralgirdle. These individuals may also demonstratedirect mechanical derangement of the internalfascial structureof the thoracic cage and intraosse-ous dysfunction of the ribs and sternum. A diaphrag-matic dysfunction is almost always associated with

this condition. In pectus carinatum, similar mecha-nisms exist but with a tendency for SBS flexion.


The evaluation of the patient commences by exam-ining the interrelationship between the sternum andthe thoracic spine, and between the sternum and theocciput. Next, examine all myofascial structuresattached to the sternum, including the pectoralgirdle and the diaphragm. The anterior abdominal

wall should be evaluated for dysfunctional tension,and, if present, contributory mechanics should besought out in the lumbar spine, sacrum and pelvis.Visceral abdominal dysfunction should also beconsidered.

Treatment consists of myofascial release appliedto identified dysfunctions. If possible, molding pro-cedures directed at the sternum should be employedsimultaneously with the myofascial release modali-ties to enhance the efficacy of both. The application

of these procedures should be done in synchronywith, and with the intent to enhance, the inherentmotility of the body. The younger the patient whentreatment is initiated, the greater the potential forpositive outcome.

VERTEBRAL SOMATICDYSFUNCTION

Vertebral somatic dysfunction in infants and chil-dren can be found at any level of the spine. It willhowever, be more commonly encountered in thelumbar, upper thoracic and cervical regions. Itusually results from the day-to-day physical activitiesand traumas of childhood. In younger children, dys-function in the cervical region will often present ascervical pain and, eventually, as torticollis. In thelumbar region, somatic dysfunction may remain qui-escent for a protracted period, in time manifestingthrough a somatovisceral mechanism as abdominapain. In older children and adolescents, the initiacomplaint from vertebral dysfunction is usuallylocalized or referred musculoskeletal pain. Becauseof the young patients ability to compensate forsomatic dysfunction, any vertebral somatic dysfunction should be thoroughly evaluated to rule out aviscerosomatic origin.

The mechanics of vertebral somatic dysfunctionmanifest in children and adolescents is the same asthat encountered in adults, showing the coupled

relationships between flexionextension, sidebending and rotation as described by Fryette.116Howeverbecause of the flexibility of the soft tissues in theseyoung patients, dysfunctional barriers are more com-pliant, lending to the application of indirect tech-niques in their treatment.

Somatic dysfunction may also exist as a reflexmanifestation of visceral dysfunction and diseaseAlthough the precise locations of viscerosomaticreflexes in infants and young children have not beenspecifically reported, it is reasonable to anticipatelocations similar to those in adults. The facilitated

state of the segmental spinal cord in the presence ovisceral input can, in turn, result in a somatovisceraresponse. A listing of viscerosomatic locations asthey have been reported in the osteopathic litera-ture is summarized in Box 7.1.1.

Because of the growth potential of these patientsvertebral somatic dysfunction can exert disproportionate impact on their developing postureas well as on the viscera through somatoviscerareflexes.




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Box 7.1.1

VISCEROSOMATIC REFLEXES

The following locations are summarized from a reviewof the osteopathic literature.117123

Eyes, ears, nose, and throat: The sympathetic reflex isT1T5. The trigeminal nerve is the final common

pathway for both sympathetic and parasympatheticinnervation of the upper respiratory tract. Themuscles of mastication, commonly the temporalismuscles, receive motor innervation from thetrigeminal nerve and serve as the somatic componentfor the upper respiratory tract sympathetic andparasympathetic reflexes. An additional reflex site isocciputC2. This results from a reflex between thetrigeminal nerve and upper cervical nerves.123

Heart: The sympathetic reflex is T1T5, left-sidedgreater than right. The parasympathetic reflex isvagal, occiput, C1, C2.

Lung: The sympathetic reflex is bilateral from T1

to T4. Conditions involving both lungs result inbilateral reflex findings. Conditions involving onelung result in a reflex on the same side as theinvolved lung. The parasympathetic reflex is vagal,occiput, C1, C2.

Gastrointestinal tract: The parasympathetic reflex from the gastrointes-

tinal tract proximal to the mid-transverse colonis vagal, occiput, C1, C2; the parasympatheticreflex from the distal half of the transverse colonto the rectum is sacropelvic S2S4

The esophagus has a right-sided sympatheticreflex from T3 to T6

The stomach has a left-sided sympathetic reflexfrom T5 to T10

The duodenum has a right-sided sympatheticreflex from T6 to T8

The small intestine sympathetic reflex isbilateral from T8 to T10

The appendix and cecum sympathetic reflex isfrom T9 to T12 on the right

The ascending colon sympathetic reflex is fromT11 to L1 on the right

The descending colon to rectum sympatheticreflex is from L1 to L3 on the left.

Pancreas: The sympathetic reflex may be left-sidedor bilateral and is T5T9. The parasympatheticreflex is vagal, occiput, C1, C2.

Liver and gallbladder: The sympathetic reflex isright-sided from T5 to T10. The parasympathetic

reflex is vagal, occiput, C1, C2. Spleen: The sympathetic reflex is left-sided from T7to T9.

Kidney: The sympathetic reflex is on the same sideas the involved kidney, from T9 to L1. Theparasympathetic reflex is vagal, occiput, C1, C2.

Urinary bladder: The sympathetic reflex is bilateralfrom T11 to L3. The parasympathetic reflex issacropelvic, S2S4.

Ovaries (and testes): The sympathetic reflex is on thesame side as the involved organ from T10 to T11.

Adrenal glands: The sympathetic reflex is on thesame side as the involved gland from T8 to T10.




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79. Magoun HI. Osteopathy in the cranial field. Kirksville, MO:The Journal Printing Company; 1951:112.

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81. Dunn PM. Congenital postural scoliosis. Arch Dis Child1973;48(8):654.

82. James JI. The management of infants with scoliosis. J BoneJoint Surg 1975;57B(4):4229.

83. McMaster MJ. Infantile idiopathic scoliosis: can it be pre-vented? J Bone Joint Surg 1983;65B(5):6127.

84. Ventura N, Huguet R, Ey A, Montaner A, Lizarraga I, VivesE. Infantile idiopathic scoliosis in the newborn. Int Orthop1998;22(2):826.

85. James JI. The etiology of scoliosis. J Bone Joint Surg1970;52B(3):4109.

86. Arbuckle BE. Scoliosis capitis. J Am Osteopath Assoc1970;70(2):1317.

87. Mohanty S, Kumar N. Patterns of presentation of congeni-tal scoliosis. J Orthop Surg (Hong Kong) 2000;8(2):337.

88. Dobbs MB, Lenke LG, Szymanski DA et al. Prevalence ofneural axis abnormalities in patients with infantile idio-

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90. Harrenstein RJ. Die Skoliose bei Suglingen und ihreBehandlung. Z Orthop Chir 1930;52:140.

91. Mehta MH. The ribvertebra angle in the early diagnosisbetween resolving and progressive infantile scoliosis. J Bone

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CN. Long-term observation and management of resolvinginfantile idiopathic scoliosis: a 25-year follow-up. J Bone

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tural scoliosis. J Bone Joint Surg 1959;41B:71935.

94. Lloyd-Roberts GC, Pilcher MF. Structural idiopathic scoli-osis in infancy: a study of the natural history of 100 patients.

J Bone Joint Surg 1965;47:5203. 95. Stehbens WE, Cooper RL. Regression of juvenile idiopathic

scoliosis. Exp Mol Pathol 2003;74(3):32635. 96. Guillaumat M, Khouri N. Scoliose idiopathique en priode

de croissance. Encycl Md Chir (Editions Scientifiques etMdicales, Elsevier SAS, Paris), Pdiatrie 2000;4007-B-20.

97. Browne D. Congenital postural scoliosis. Br Med J 1965;5461:5656.

98. Reamy BV, Slakey JB. Adolescent idiopathic scoliosis:review and current concepts. Am Fam Physician 2001;64(1):1116.

99. Escalada F, Marco E, Duarte E et al. Growth and curve sta-

bilization in girls with adolescent idiopathic scoliosis. Spine2005;30(4):4117.

100. Edgar MA, Mehta MH. Long-term follow-up of fused andunfused idiopathic scoliosis. J Bone Joint Surg 1988;70B(5):7126.

101. Morin C. Traitement des scolioses idiopathiques chezlenfant en priode de croissance. Bull Acad Natl Med 1999;183(4):7315.

102. Rowe DE, Bernstein SM, Riddick MF, Adler F, Emans JB,Gardner-Bonneau D. A meta-analysis of the efficacy of non-operative treatments for idiopathic scoliosis. J Bone JointSurg 1997;79(5):66474.

103. Donnelly MJ, Dolan LA, Weinstein SL. How effective isbracing for treatment of scoliosis? Am Fam Physician2003;67(1):32, 35; author reply 35.

104. Niesluchowski W, Dabrowska A, Kedzior K, Zagrajek T.The potential role of brain asymmetry in the developmentof adolescent idiopathic scoliosis: a hypothesis. J ManipPhysiol Ther 1999;22(8):5404.

105. Morningstar MW, Woggon D, Lawrence G. Scoliosis treat-ment using a combination of manipulative and rehabilita-tive therapy: a retrospective case series. BMC MusculoskeletDisord 2004;5:32.

106. Hawes MC. The use of exercises in the treatment of scolio-sis: an evidence-based critical review of the literature.Pediatr Rehabil 2003;6(34):17182.

107. Lonstein JE. Congenital spine deformities: scoliosis, kypho-sis, and lordosis. Orthop Clin North Am 1999;30(3):387405, viii.




108. Deacon P, Berkin CR, Dickson RA. Combined idiopathickyphosis and scoliosis. An analysis of the lateral spinal cur-vatures associated with Scheuermanns disease. J Bone JointSurg 1985;67B(2):18992.

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112. Nissinen M. Spinal posture during pubertal growth. ActaPaediatr 1995;84(3):30812.

113. Willner S, Johnson B. Thoracic kyphosis and lumbar lordo-sis during the growth period in children. Acta PaediatrScand 1983;72(6):8738.

114. Labelle H, Roussouly P, Berthonnaud E, Dimnet J,OBrien M. The importance of spino-pelvic balance inL5S1 developmental spondylolisthesis: a review of perti-nent radiologic measurements. Spine 2005;30(6 Suppl):

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7.2 APPENDICULAR IMBALANCE

Upper extremity

FRACTURES OF THE CLAVICLE

The clavicle is the bone most frequently fracturedduring the birth process. Clavicular fractures occurin about 1.6% of all vaginal deliveries1,2 and 0.5%when considering all live births.3 Both males andfemales are affected equally, with equal left versusright-sided incidence.3There is, however, a slightlyincreased incidence of right-sided fractures in leftocciput-anterior deliveries.4

Reported risk factors for clavicular fracturesinclude increased duration of the second stage oflabor, increased birth weight and neonatal length

(macrosomia), instrumental delivery2and shoulderdystocia.3In cephalic presentation, the compressionof the infants anterior shoulder against the maternalsymphysis is responsible for the trauma.4Direct pres-sure or torsion applied to the clavicles to facilitatedelivery can also result in fracture.

Complete or incomplete greenstick fractures aremost frequent. They present with edema, crepitus, apalpable bony bump and tissue texture changes overthe fracture site. Decreased or absent movement ofthe affected arm is present, as may become apparentwhen eliciting the Moro reflex. Asymptomatic or

incomplete clavicular fractures may not be initiallyidentified until after discharge from the hospitalUsually, the caregiver will notice that the child dem

onstrates irritability with discomfort and pain whenputting the childs arm through the sleeve of agarment or when lifting the child by holding themunder their arms. They are also liable to report thatthe child cries when positioned on the affected side

Shoulder dislocation, humeral fracture and bra-chial plexus injury are part of the differential diag-noses. The diagnosis is confirmed radiographicallyAssociated complications, such as Erbs palsy, arepresent in 11.3% of newborns with fractures of theclavicle,2although clavicular fracture may actuallyreduce the potential nerve injury from traction on

the brachial plexus.4Usually no orthopedic treatment is necessary for

asymptomatic and incomplete clavicular fracturesWhen the neonate presents with pain or discomfortthe affected arm may be immobilized by pinning thesleeve to the front of the shirt for 710 days.5A largecallus typically forms at the fracture site within aweek, and recovery is usually considered to becomplete. Osteopathic procedures may be employedto assist the recovery process and address the dys-functions usually associated with a fracture of theclavicle.




The clavicle is of importance because of its myofas-cial attachments. It serves as a junction between thefasciae of the thorax, arm and neck. The investinglayer of the deep cervical fascia completely surroundsthe neck. Superiorly, it is attached to the externaloccipital protuberance and the superior nuchal line,the mastoid processes, zygomatic arches and the infe-rior borders of mandible. It splits to surround the tra-pezius and sternocleidomastoid muscles. Inferiorly, itis attached to the manubrium of the sternum, theacromion and the spine of the scapula.

The clavicle is the link in the fascial continuitybetween the investing layer of the deep cervical fasciaand the fascia of the thorax and the arm. The clavi-pectoral fascia attaches on the clavicle, as does thedeltoid fascia. The deltoid fascia is in continuity withthe brachial fascia. The clavicle, therefore, plays animportant role in the equilibrium of the fascia of thethorax, arm and neck, and should be balanced, asshould the myofascial structures attached to it.

Forces applied during the delivery that are greatenough to fracture the clavicle also affect the neckand upper thoracic vertebrae of the neonate. There-fore the osteopathic practitioner should evaluatethese structures and treat any dysfunctions accord-ingly, using indirect principles.

Furthermore, because of pain from the fracturedclavicle, the child will prefer to lie on the oppositeside, thereby fostering the development of asym-metric fascial tensions. These asymmetries can, inturn, induce the child to select a chronic position of

comfort, long after the clavicle has healed. Thechronic asymmetric positioning can then predisposethe child to the development of plagiocephaly.

Fractures of the clavicle that occur during child-hood are usually the result of rough play or athleticactivities. In childhood, the forces that result inclavicular fractures are usually violent, most ofteninvolving impact on the hand with the arm extendedor impact on the shoulder. In 75% of cases the siteof fracture involves the medial third of the bone.The standard orthopedic treatment reduces the dis-placement at the fracture site by maintaining the

shoulder in an upward and backward position witha bandage or plaster.


Osteopathic procedures applied to the older childfollow the same anatomic principles as for the infant,i.e. to alleviate myofascial imbalances and upperthoracic and cervical dysfunction. The acromiocla-vicular junction may demonstrate somatic dysfunc-tion; it should, therefore, be evaluated and treatedfollowing indirect principles. It is of importance to

allow for normal function of the growing upperextremity. Acromioclavicular dysfunction is thesource of many adult shoulder disorders.

BRACHIAL PLEXUS INJURY

A brachial plexus injury occurs most commonly asa result of a difficult birth, fetal malpresentation,5shoulder dystocia, macrosomia6 or assisted vaginaldelivery.7 Fracture of the clavicle(s) or humerus,8shoulder dislocation, torticollis, hematomas of thesternocleidomastoid muscle or paralysis of the dia-phragm may be associated with injury of the brachialplexus.5

A commonly believed etiology of brachial plexusinjury is excessive traction on the fetal head duringbirth. In vaginal delivery, during the attempt todeliver the anterior shoulder, the applied downward

traction can damage the brachial plexus. This theory,however, is questionable because, in almost half thecases of brachial plexus injury, delivery of the shoul-ders occurs without difficulty. Therefore, an in utero,atraumatic theory is also proposed.8When asymme-try and diminished movement of the arm areobserved on the fetal ultrasound, a vulnerable plexusmay be injured without traction during delivery.9

The brachial plexus is formed by the union of theanterior divisions of the lower four cervical nervesand part of the anterior division of the first thoracicnerve. In addition, the fifth cervical nerve frequently

receives a branch from the fourth cervical, and thefirst thoracic a branch from the second thoracic. Theplexus extends from the inferior aspect of the side ofthe neck to the axilla. The fifth and sixth cervicalnerves unite to form the upper trunk; the eighthcervical and first thoracic nerves form the lowertrunk, while the seventh cervical nerve runs outalone as the middle trunk. These three trunks passbeneath the clavicle and split into the anterior andposterior divisions. The plexus is attached to the firstrib and to the coracoid process by the costocoracoidmembrane and is subject to any force that disturbs

the relationship between the cervical vertebrae, thefirst thoracic vertebra and ribs, the clavicle and thescapula (Fig. 7.2.1).

Most of the time brachial plexus injury is unilat-eral and immediately recognizable. Brachial plexusinjury can affect different spinal nerve roots and isidentified as follows:

Upper type, with involvement of C5 and C6, orErbDuchenne palsy that affects muscles of theshoulder and elbow. The child presents withadduction of the upper extremity and internal




rotation of the shoulder, but grasp remainsintact. It represents most of the brachial plexusparalyses10and is considered to have a goodprognosis.

Lower type, with involvement of C7, C8 andT1, or Klumpkes palsy that affects muscles ofthe forearm and hand. The child presents with

a paralysis of the hand and wrist. The presenceof an ipsilateral Horners syndrome (anhidrosis,miosis and ptosis) indicates an involvement ofthe sympathetic fibers associated with anintraspinal avulsion of the root of T1.

Whole arm type, with involvement of C5T1,with no movement of the upper extremity andoften associated with sensory loss.

Extreme lateral flexion and traction of the headmay be responsible for the stretch applied to thebrachial plexus. The injury results in anything from

a mild edema or hemorrhage within the affectednerves, to tearing of the nerve(s) that could be asextensive as to produce a total avulsion of the com-plete plexus. The C5 and C6 spinal nerves arelocated in the sulcus nervi spinali of the transverseprocesses. In that location they are strongly attachedby various fibrous slips as extensions of the prever-tebral fascia and surrounding structures attached tothe spinous processes, and are, therefore, more likelyto be ruptured.11The C8 and T1 spinal nerves may,more often, be subject to avulsion.11

Neuronal injury associated with brachial plexuinjury may be of different degrees of severity:

Neuropraxic lesions are failure of conductionwithout the axon having been affected, and arereversible.

Axonotmetic lesions involve disruption of both

the myelin sheath and the axon, but with thesurrounding neuronal elements kept intact.Wallerian degeneration of the axon distal to theinjury occurs.

Neurotmetic lesions are total sectioning of thenerve with its myelin sheath and supportingconnective tissue.

Avulsion is a separation of the plexus from thespinal cord.

Obstetric brachial plexus palsy occurs in 0.42.5per 1000 live births with an upper root (C5C6)involvement in 50% of cases; C5, C6 and C7

involvement in 25%; and the whole plexus in25%.6,8,12Neuropraxic and axonotmetic lesions havebetter prognoses.


The diagnosis is made by physical examination. TheMoro reflex is asymmetric and the biceps deeptendon reflex is absent. The grasp reflex is, howevernormal. The child should be moved very gentlythe injuries are painful and the tissues very fragileInitial treatment is usually conservative with regula

Superiorsubscapular nerve

Terminalnerves

Cords Divisions Trunks Roots(anterior rami)

C5

C6

C7

C8

T1

Superior

Middle

Inferior

Lateral

Posterior

Medial

Anterior

Anterior

Lateral pectoral nerve

Medial pectoral

Medial cutaneous nerve of arm

Medial cutaneous nerve of forearm

Musculocutaneous

Median

Radial

Ulnar

Axillary

Long thoracicnerve

Suprascapular nerveDorsal scapular nerve

Contributionto phrenic

nerve

Nerve to subclavius

Thoracodorsal nerve

Inferior subscapular nerve

Posterior

Posterior

Poste

rior

Anterior

Figure 7.2.1. Branches of the brachialplexus.




assessment. If the patient fails to show significantimprovement by 3 months of age, surgical opinionshould be sought.13

Physical therapy, consisting of gentle passivemobilization, may be employed to maintain range ofmotion and prevent contractures while the infant isrecovering active motion. Specific motor trainingcan be initiated within the first 2 weeks, with facili-tation of active movement. The persistent neuro-logic deficits may result in the development ofinternal rotation and adduction contractures of thearm. Gentle stretching of internal rotators should beperformed to reduce this risk while avoiding rein-forcement of forearm supination.

Osteopathic procedures should be employed asearly as possible in the treatment of brachial plexusinjury. Traumatic forces may have injured the bra-chial plexus, but other areas, such as the upper tho-racic spine, the first rib, the cervical spine, clavicleand all of the myofascial components of the thoracicoutlet, have been stressed as well. Dysautonomiamay also be present because somatic dysfunction ofthe cranial base and occipitoatlantal region canaffect the parasympathetic tone through the vagusnerve, while somatic dysfunction in the upper tho-racic spine can affect sympathetic nervous function.Direct compression of the venous and lymphaticdrainage of the brachial plexus, as well as somatovi-sceral reflexes, should be considered when attempt-ing to facilitate nerve regeneration. Osteopathicprocedures aim to promote fluid, electrolyte and

metabolic exchange within the tissues to facilitatedrainage of edema and to prevent or reduce tissuescarring. Treatment is intended to optimize nerveregeneration and prevent the development of mus-cular imbalance. Recuperation of the commonmotor deficits, such as the absence of active externalrotation, flexion and abduction of the shoulder, andfunction of the biceps should be addressed to mini-mize bony deformities and joint contractures.

The neonate with possible brachial plexus injurymay be examined on the treatment table. Observefor spontaneous movements of the head, trunk,

pelvis and limbs. Check for subtle facial palsy thatmay be found as a concomitant result of birth trauma.Inspect shoulders and limbs for deformities. Evaluaterange of motion of every joint of the affected limb.Palpate for tissue texture changes in the upperextremities. Look for signs of shoulder instabilitysuch as a palpable or audible click during movement.Palpate for tissue texture changes in the suboccipi-tal, neck and upper thoracic areas. The connectivetissues are responsible for the maintenance ofshape against both external and internal stresses.14

Mechanical forces contribute to the developmentand evolution of the extracellular matrices found inthe connective tissues.15As tissue texture changesfollow trauma, osteopathic procedures should helpin resetting structure and function of traumatizedconnective tissues.

Evaluate, through tests of listening, the function ofthe humerus, scapula, clavicle, sternum, upper tho-racic spine, first ribs, cervical spine and craniocervicaljoints. This method of assessment is of particularvalue with this type of pathology because it is sogentle. Anatomic visualization is, as always, impor-tant. As you evaluate the patient, visualize the differ-ent layers of soft tissue: fascia superficialis, cervicalfascia, costocoracoid membrane, sternocleidomastoidand scalene muscles. Evaluate and visualize the differ-ent bones involved. Listen to the inherent motions inorder to define the dysfunctional area. Study the rela-tionship between the shoulder and the vertebralcolumn. For instance, in the case of a Klumpkes palsy,place the pad of the fingers of one hand on the spinousprocesses of C6, C7, T1 and T2, and place the otherhand on the ipsilateral shoulder. Listen, and look fordysfunctional motion. One vertebral segment may bemore dysfunctional than others. The relationshipbetween the humerus and the shoulder should also bebalanced. Treat the dysfunctions you identify byapplying indirect principles.

Improvement should be rapid and most cases havea favorable prognosis. Injuries involving the fifthand sixth cervical nerve roots have the best progno-

sis, whereas lower plexus and total plexus injurieshave a poorer prognosis. Significant deficit persistingafter 3 months should be explored surgically. Prog-nosis is excellent if antigravity movement of bicepsand shoulder abductor is present by 3 months of age.Assessment may be performed by testing the bicepsstrength in a supine position while simultaneouslypalpating the muscle. Bicipital activity should notbe confused with flexion of the elbow obtained bythe action of the supinator muscle. Surgery is con-sidered by some authors when antigravity movementof the biceps is not present by 3 months of age.16

Surgery is considered to be justified by others whenan initial involvement of the C7 nerve root ispresent, with a birth weight above the 90th percen-tile and there is only poor elbow flexion at 6 and 9months of age.12

SHOULDER DYSPLASIA

The plasticity of the glenohumeral joint in thenewborn makes it subject to shoulder dysplasia and,




in more severe cases, dislocation. These disordersmay be compared to similar disorders occurring inthe hip joint hip dysplasia and hip dislocation and in some cases the etiology may be similar.

Intrauterine forces applied to the fetus can resultin shoulder dysplasia. During the latter part of preg-nancy any compression of the upper fetal torsowithin the uterus may affect the glenohumeral jointand the surrounding soft tissues.

Stresses during the birth process can also contrib-ute to the development of shoulder dysplasia.Increased duration of the second stage of labor,greater than 2 hours, has been described as a factorcontributing to shoulder dystocia.17 Additionally,macrosomia that results in a size discrepancy betweenthe fetal shoulders and the maternal pelvic inlet can,in severe cases, lead to significant neonatal morbid-ity including asphyxia and trauma, particularly tothe brachial plexus. A large fetal trunk, or increasedbisacromial diameter, prevents the rotation of thefetal shoulders into the oblique pelvic diameterduring delivery.18As a consequence, certain obstet-rical maneuvers may have to be employed to allevi-ate the impaction of the fetal shoulders within thematernal pelvis.19As stressful as such a dispropor-tionate relationship between the fetus and thematernal pelvis can be, it does not always result inovert trauma to the brachial plexus. It can, however,cause injury to the shoulder that can lead to shoul-der dysplasia. This type of injury to the shoulder canoccur even from the stresses of an otherwise normal

delivery.Dysplasia of the shoulder may also result from

postpartum conditions. The presence of dysfunc-tional asymmetries in the newborn, congenital mus-cular torticollis, non-synostotic plagiocephaly andbrachial plexus injuries may contribute to abnormaldevelopment of the glenohumeral joint. Contrac-tures of the muscles of internal rotation in neonatalbrachial plexus palsy are responsible for posteriordislocation of the humerus from the glenoidfossa,2022requiring orthopedic repair.

Physical examination and treatmentMilder cases of dysplasia without dislocation may betreated using osteopathic procedures. If untreated,these glenohumeral dysfunctions can increase withage, becoming the cause of adult scapulothoracicproblems. Therefore, the scapula and the glenohu-meral joint should be evaluated at birth for any signsof dysplasia, as precisely as the pelvis is evaluated.Particular attention should be directed at the identi-fication of signs of shoulder instability, such as a pal-pable or audible click during movement. Observe

and compare the size and shape of both shouldersThe examination may reveal asymmetry in thenumber of skin folds in the proximal part of the armsObserve the freedom and range of motion of bothshoulders. Note any restriction, stiffness of move-ment and asymmetry in movement, particularlyexternal rotation and abduction of the arm. Themalposition of the humeral head may result in anapparent difference in the length of the arms, withthe arm on the side of the dysplasia appearing to beshorter. Compare the anterior and posterior aspectsof the shoulders and look for any posterior fullnessthat may be indicative of a posteriorly displacedhumeral head, necessitating orthopedic attention.

Treat any somatic dysfunction identified usingindirect principles. Stabilization of the humerahead in the glenoid fossa may be facilitated whenmyofascial procedures are applied to the periarticu-lar muscles of the shoulder.

NURSEMAIDS ELBOW

Nursemaids elbow, also called pulled elbow, is aradial head subluxation that occurs in younger children when traction is applied suddenly to their handor forearm. This commonly occurs when an adult isattempting to lift a child up by pulling upward whileholding the childs hand. Traumas such as falls orwhen the infant initiates rolling over are other possible causes of this condition.

The head of the radius articulates with the radianotch of the ulna and the surrounding annular liga-ment. Under normal conditions, the annular ligament encircles the head of the radius with a certainamount of tension that maintains the contact withthe radial notch. The normal movements of thehead of the radius, within the ring formed by theannular ligament and the radial notch of the ulnaare anterior and posterior motion. Pronation is associated with posterior radial motion and supinationwith anterior radial motion.

In nursemaids elbow a subluxation of the devel

oping radial head from the annular ligament of theelbow joint occurs. A combination of pronation andtraction on an extended elbow causes a proximal slipof the annular ligament over the top of the radiahead with resultant interposition of some fibers othe anterior joint capsule between the two bones.23


The most common symptoms of nursemaids elboware immediate pain and an inability to move thearm. The child will have a partially flexed elbow




with pronation of the forearm. Most of the timeanxiety is also present.

The intention of osteopathic treatment is torestore motion between the head of the radius andthe radial notch of the ulna and surrounding annularligament. Ligamentous articular strains may be bal-anced utilizing indirect principles that apply per-fectly to this condition. Balancing the annularligament and the radial collateral ligament of theelbow may prevent recurrence of a posterior radialhead subluxation. The caregiver should be told toavoid pulling or lifting their child by the arms orhands.

Lower extremity

A frequent complaint in an osteopathic practice isintoeing, i.e. the childs feet turn in when walking

or running. Malposition of the feet, developmentaldysplasia of the hip and toe walking are among theother complaints encountered with infants, whilesprains are more frequently encountered with theolder children and teenagers.

DYSFUNCTIONS OF THE FEET

Metatarsus adductus

Metatarsus adductus is an adduction of the forefootthat occurs in 1 : 5000 live births.24The classic view

of it resulting from intrauterine positioning isdebated, since genetic factors may contribute.25Sleeping in the prone position also seems to promoteit. This is a frequent cause of intoeing during thefirst year of life and is more frequently encounteredon the left side.24Normally, in the neutral position,the heel-bisector line drawn through the midlineaxis of the hindfoot passes through the forefoot atthe second web space. In cases of metatarsus adduc-tus, the line passes lateral to the third toe. Therefore,an angulation exists medially between the forefoot,or metatarsals, and the hindfoot. Sometimes a trans-

verse crease is present on the medial side of the footand the lateral border of the foot is convex (Fig.7.2.2).

Metatarsus adductus associated with an inversionof the foot is named metatarsus varus and adductionof the first metatarsal is metatarsus primus varus.Metatarsus adductus is frequently associated withinternal tibial torsion. Metatarsus adductus associ-ated with retracted equinus the inability to dorsi-flex at the ankle is indicative of a diagnosis ofclubfoot.

Dysfunctions of the feet might not seem grave,but left untreated they will lead to postural dysfunc-

tions and compensatory dysfunctions of the feet,with difficulty wearing shoes and the developmentof bunions and hammer toes. A group of childrenwith metatarsus varus, followed an average of 7years, showed that 10% maintained a moderate,although asymptomatic, deformity and 4% demon-strated residual deformity and dysfunction (stiff-ness).25The opinion is that metatarsus adductus leftuntreated will persist into adulthood in 45% ofcases.26,27Furthermore, some cases only appear to beclinically improved because of a compensatory pro-nation of the midtarsal joints and rearfoot.28

Metatarsus adductus is classified according to itsflexibility. Normally, an infant should extend andabduct the foot when being tickled (e.g. with atoothbrush) along the lateral border of the foot,particularly over the fifth metatarsal head. Theinability of the infant to react in such a way isindicative of metatarsus adductus. The physicianshould consider the total body approach and treatany dysfunctional mechanics, particularly ofLisfrancs joints (tarsometatarsal) following theprinciples of functional procedures. The parentsshould be encouraged to stimulate abduction of the

forefoot, using a toothbrush or similar stimulus, asdescribed above. In more severe cases it should beproposed that stretching exercises be practicedseveral times a day (e.g. at each diaper change). Thecalcaneus is maintained between the thumb andindex finger, while the forefoot is gently pulled intoa corrected position, holding the correction for 10seconds and repeating the process about five times.It should be stressed that this exercise should bedone properly, without creating a valgus of the hind-foot. If these treatments fail, and also in cases of

Figure 7.2.2. Metatarsus adductus of the right foot.




severely rigid feet, a series of casts are used to gradu-ally straighten out the deformity.

Congenital idiopathic talipesequinovarus (CTEV)

CTEV, or clubfoot, is a complex deformity ofunknown pathogenesis with several etiologichypotheses that range from genetic to intrauterinefactors.29The headbody angle of the talus (declina-tion angle) which normally increases after the 16thweek of gestation has been found to be decreased inCTEV, associated with hypoplasia of the talus.30More recently, studies indicate that talar deformityis notthe primary lesion, but follows loss of spatialorientation of the deltoid and spring ligaments andtibialis posterior tendon insertion, with contractedsoft tissues.31

CTEV is a relatively common congenital defor-mity that occurs with geographical differencesranging from 0.5 : 1000 live births in Japan to 7 : 1000in the South Pacific (1.2 : 1000 live births amongCaucasians).32About 50% of the cases are bilateral.The male-to-female ratio for affected children is2.5 : 1.32,33

Clubfoot deformity presents with different com-ponents: hindfoot equinus (inability to dorsiflex),hindfoot varus and metatarsus adductus. The flexi-bility of the deformity is important to determine thedegree of severity. Classic treatment consists ofmanipulation of the foot followed by casting.34Gen-

erally, casting is attempted for 3 months; if unsuc-cessful, surgery is planned.

Osteopathic procedures should be employed asearly as possible for best results. Every bone ofthe hindfoot the calcaneus, talus, navicular andcuboid bones should be evaluated and treated torelease any dysfunctional relationships betweenthem and to equilibrate the soft tissues surroundingthem. The deltoid and plantar calcaneonavicular(spring) ligaments are of particular importanceand should be balanced with gentle fascial releaseprocedures.

Pes cavus

Pes cavus, or high-arched or hollow foot, should firstmake you think of ruling out an underlying neuro-logic disorder as the primary etiology. Anterior pescavus, where both the medial and lateral longitudi-nal arches are high, is benign. Medial pes cavus ismore severe, often with claw foot deformity of thetoes. The two may be differentiated by dorsiflexingthe foot. In the presence of medial pes cavus the

claw foot deformity of the toes increases with dorsi-flexion of the foot.

The position and range of motion of the hindfootbones, particularly the talus, should be evaluatedHollow foot is often associated with a flexionexternal rotation pattern of the craniosacramechanism.

You must differentiate total flat foot or totahollow foot from partially flat foot or partially hollowfoot. In the latter, only the posterior portion of thelongitudinal arch is involved, resulting from animbalance of the subtalar, calcaneocuboid or cuneo-cuboid articulation.

Pes planus (flat feet)

A rigid pes planus is a pathologic flat foot, alsonamed tarsal coalition, in which one or more of thetarsal bones that should have a joint between thembecome fused. In infants the fused joints are cartilaginous and are still relatively flexible. Thus thecondition is typically not symptomatic beforeadolescence.

Physiologic pes planus is a loss or reduction ofthe longitudinal arch (Fig. 7.2.3) that can be reestablished when the child stands on their toesPhysiologic pes planus is flexible and often associ-ated with generalized ligamentous laxity. In a sampleof primary school children, 2.7% demonstrated flatfeet, and being overweight was shown to increasethe prevalence of the condition.35Because of liga-

mentous laxity and/or obesity, the childs anklescave in.

The plantar calcaneonavicular ligament playsan important role in maintaining the arch of thefoot (Fig. 7.2.4). It supports the head of the talusand is part of the astragalonavicular joint. Anydysfunction of the plantar calcaneonavicular liga-ment affects the head of the talus that tends to bedisplaced downward, medially and forward by theweight of the body. The tibialis posterior, aninversion muscle, lies directly below the plantarcalcaneonavicular ligament and participates con

siderably in maintaining the longitudinal arch othe foot. In cases of dysfunction of these structuresthe foot becomes flattened, expanded and turnedlaterally.

This condition has been suggested as a cause fortarsal tunnel syndrome.28It has also been suggestedas contributing to back and knee problems later inlife, but no evidence supports this contention. Flatfeet and dysfunction of the spine are, however, veryoften two components of the same problem, wherepostural mechanics are involved. Flat foot is usually




associated with an extensioninternal rotationpattern of the craniosacral mechanism.

The treatment of physiologic pes planus withorthotic devices is controversial.36Insole arch sup-ports diminish some of the muscular activity thatmaintains the arch and tend to weaken the muscles.35Two studies suggest an association between wearingshoes at an early age and flat feet.37,38This stressesthe importance of allowing the feet to grow anddevelop without constraint. Parents should be reas-

sured about their concerns regarding the childsappearance and gait. This condition tends to improvebetween 2 and 6 years of age.39To promote optimalgrowth without dysfunctional mechanics, the osteo-pathic practitioner should consider the globalposture of the child. Check for rearfoot valgus byassessing the position and freedom of the calcaneusand talus. Check also for internal rotation dysfunc-tion of any of the tarsal bones. Encourage the child,through their parents, to maintain a healthy life-style, to go barefoot as much as possible and not

to become overweight. Physical activities thatstrengthen foot inversion, such as walking on thelateral borders of the feet or picking objects withthe toes, should be recommended.

Calcaneovalgus

Positional calcaneovalgus, the result of intrauterinemalposition, is a flexible dorsiflexion of the anklewith a mild subtalar joint eversion. It is frequently

associated with external tibial torsion and has theappearance of flat feet. Treatment follows the prin-ciples of functional procedures to address the subta-lar dysfunction.

Sprains and strains

Sprains and strains are common in the pediatricpopulation. Young athletes are particularly vulnera-ble. Activities that involve jumping and landing, asin skateboarding, often result in such injuries. These

Medial longitudinal arch

Lateral longitudinal archTransverse arch

Figure 7.2.3.Arches of the right foot.

Plantar calcaneonavicular ligament

Long plantar ligamentShort plantar ligamentPlantar aponeurosisFigure 7.2.4. Support for the arches of thefoot.




injuries are, however, not limited to young athletes.Young children can sustain sprains and strains withactivities of daily living, such as ascending ordescending stairs. These injuries may be overlookedbecause of the childs tendency to get up and resumeactivity unless severely injured; however, if notproperly addressed, such injuries can be the sourceof functional asymmetry and somatic dysfunction,often with sequelae in other anatomic areas at a laterdate. Following a foot or ankle sprain that causes

excessive or prolonged midfoot pronation, abnormalpatellofemoral mechanics may result.40

Traumatic twisting of the forefoot, most ofteninversion, commonly causes ankle injuries, oftenresulting in, but not limited to, sprains or strainsinvolving the tibia, fibula and talus. It should beremembered that these stresses may also result inspecific dysfunctions between the fibula and talus,the talus and calcaneus, the talus and navicularbone, and the calcaneus and cuboid, as well as dys-functions between any of the other adjacent tarsaland metatarsal bones (Figs 7.2.5, 7.2.6).

On physical examination, the acutely injuredankle presents with pain and swelling and, withmore severe injuries, ecchymosis. Ecchymosis indi-cates possible ligamentous tears or bony fracturenecessitating radiographic evaluation. Further, if thesubject is not willing to bear weight on the injuredankle, or if significant edema is present, radiographicevaluation is also appropriate to evaluate the extentof injury.41

Once bony fracture has been ruled out, soft tissueinjuries may be treated with osteopathic manipula-

tion by employing indirect principles. Under thesecircumstances, the patient should experience noaggravation of discomfort during the treatment pro-cedure and will often feel a significant reduction opain and swelling following the intervention. Post-

treatment reduced weight bearing and avoidance ostressful activities should be recommended. Immo-bilization of the injured area with strapping methodshould be considered for adolescents and individuallikely to be involved in weight-bearing activitiesWhen there is no more pain for a week, a rehabilita-tion program can be organized to work the injuredankle in full range of motion with progressive resis-tance exercises. Exercises with a balance board, tostrengthen proprioception, function and coordination, are also indicated. The patient places the footon the board and first does flexionextension move-

ments, followed by rotation of the ankle around theball (Fig. 7.2.7).

DYSFUNCTIONS OF THE LEGS

Tibial torsion

A thorough history and physical examination shouldbe performed to rule out diagnoses such as cerebralpalsy, which can present with rotational misalign-ment of the legs. Internal tibial torsion is said to be

Anterior talofibular ligament

Calcaneofibular ligament

Posteriortalofibularligament

Malleolar fossa

Figure 7.2.5. Lateral view of the ankle joint.

Plantar calcaneonavicular ligament

Medialtubercleof talus

Sustentaculum talof calcaneus bone

Tuberosity ofnavicular bone

Posteriortibiotalar part

Medial ligament of the ankle joint

Tibiocalcaneal part

Tibionavicular part

Anterior tibiotalar part

Figure 7.2.6. Medial view of the ankle joint.




the result of intrauterine positioning or from thechilds habit of sitting on their feet. This is often

noticed by the parents between 1 and 2 years of ageand is a common cause of intoeing in children under3 years of age. Internal tibial torsion is more oftenbilateral; when unilateral, the deformity most com-monly affects the left side.24Parents complain thattheir child is clumsy, trips and falls easily, althoughintoeing in athletes has been suggested as beneficialin activities like sprinting.42 About 9095% of alltorsional deformities resolve spontaneously by matu-rity.43When it does not resolve, however, dysfunc-tional rotation results in improper alignment of thelower limb and is associated with arthrosis of the hip,

knee and ankle.44External tibial torsion is usually diagnosed later

and demonstrates a tendency to increase with age.It is associated with conditions of the extensor appa-ratus as unstable patellofemoral joints and OsgoodSchlatter disease.45,46

Examination of rotation of the tibia is best donewith the child in the prone position with their kneeflexed to 90. This allows measurement of the footthigh angle, the angle formed between the long axesof the femur and the foot.

The osteopathic practitioner should consider atotal body approach with specific attention tointraosseous and myofascial tensions in the lowerlimbs. The relationships between the fibula and thetibia, as well as between the tibia and the femur andthe tibia and the talus, should be balanced. Osteo-pathic procedures directed at functional alignmentand balance of the lower extremity improve func-tion and should reduce stressful compensatory pat-terns that may later result in patellar tendonitis andarthritis.

Femoral torsion

Femoral torsion is defined by the angle between thefemoral neck axis and the transcondylar axis of thedistal femur. Femoral torsion can be internal (femoralanteversion) or external (femoral retroversion) andresults in the knees pointing toward or away fromeach other, respectively. A normal femur is ante-verted, i.e. the femoral head and neck are rotatedanteriorly with respect to the femoral condyles.Babies have 30 of femoral anteversion. Thisdecreases by about 1.5per year to reach 10in adultlife.33 Femoral anteversion is also a very commoncause of intoeing in children under 3 years of age,the child being obliged to internally rotate thefemurs in order to re-center the femoral heads in theacetabula. Observation of the childs gait allows oneto differentiate between intoeing that is the resultof internal tibial torsion as compared to femoral

anteversion where the patellae are positioned moremedially on the knees. The child trips and falls fre-quently and does not like to sit with their legscrossed, preferring to sit in a W position (Fig.7.2.8). Parents note that the childs shoes are veryquickly worn out in an asymmetric pattern. Studiesin adults in whom the condition remained uncor-rected found a correlation between femoral antever-sion and arthritis of the knee.47

Normally, hip range of motion shows greateramplitude in medial rotation than in lateral rota-tion. Abnormal femoral anteversion can be pre-

dicted (2 SD from the mean) if the differencebetween medial and lateral rotation is 45 ormore.48

The osteopathic practitioner should consider atotal body approach and release intraosseous andmyofascial tension in the lower limbs. The pelvisshould be diagnosed and treated if necessary, as wellas the coxofemoral joint. Somatic dysfunction of theinnominate, particularly during periods of growth, issignificant because of the influence it can have onthe position of the femur.

Figure 7.2.7. Rehabilitation includes exercises with a balanceboard.




Genu varum and genu valgum

Genu varum and genu valgum also known asbowlegs and knock-knees, respectively are commonangular deformities of the lower extremities in chil-dren. All babies are born bowlegged. Between the

ages of 2 and 3 years the bowlegging graduallydecreases, and by 3 years the average child is maxi-mally knock-kneed. The knock-kneeing straightensminimally over the next several years and, by age 7years, most children have reached the typical adultconfiguration, which is slightly knock-kneed.

Persistent genu varum is better tolerated func-tionally than valgus, which causes stress to themedial aspect of the knee joint with the subsequentdevelopment of pain. The wider the varus or thevalgus, the greater the shear stress (lateralmedialforces) on the joint.

An angular deformity is not physiologic when itis asymmetric or painful and radiographs might benecessary. Bilateral varus is associated with cranio-sacral flexion of the sacrum, and bilateral valguswith a sacrum in craniosacral extension. Unilateralvarus problems are very often associated withflexionexternal rotation patterns on the same sideat the level of the pelvis, the temporal bone or theoccipital bone. Similarly, unilateral valgus problemsare associated with extensioninternal rotation pat-terns of these same areas.

Using indirect procedures from a total body per-spective, treatment is directed at specifically diag-nosed dysfunctional mechanics. The distancebetween the knees (with the ankles together) ofchildren who have varus, or between the ankles(with the knees together) of children who havevalgus, can be measured to follow the response totreatment.

The knee can also present minor strains. A com-monly found pattern occurs when an increasedmedial femoral torsion is combined with excessivelateral torsion of the tibia. This is found more oftenas the result of physical activities, such as in skiingwhen the ski is stuck in the snow, slightly abductedand the rest of the body moves forward. The rela-tionship between the tibia and the femur should bebalanced to address these strains.

Patellar disordersCongenital dislocation of the patella is rareand may be isolated or associated with other limbmalformations.49 Patellar instability is not a con-genital condition, although anatomic configura-tions such as patella alta, trochlear dysplasia andligamentous laxity are thought to participate in theinstability. MRI permits visualization of the non-osseous components of the patellofemoral arti-culation in the child. The cartilaginous compositionof the articulation provides less restraint to lateramovement of the patella that allows instability.4

The trilaminar soft-tissue structures50 surroundingthe patella present interconnections with thefibers of the iliotibial tract, lateral hamstrings andlateral quadriceps retinaculum. Tightness in thesestructures has been suggested as causing excessiveposterior and lateral pull, contributing to patellarinstability, especially if the medial patellofemoraligament is injured and cannot stabilize the knee.4

These structures are linked to the pelvic boneand recurrent dislocation of the patella can beassociated with pelvic dysfunctions that interferewith the balance transmission of weight-bearing

forces.OsgoodSchlatter disease occurs mainly in ath

letic adolescent boys. It is suggested that a welldeveloped and inelastic quadriceps creates a tractionapophysitis on the tibia, with the development oloose ossicles and elongation of the patellar ligamenleading to patella alta.51 Patients with OsgoodSchlatter disease also present with increased exter-nal tibial torsion that, in association with otherfactors, has been suggested to predispose to the onsetof the disease.46

Figure 7.2.8. Sitting in a W position.




The osteopathic practitioner will consider a totalbody approach and release the pelvis, the hips, theknees and the patellofemoral articulations (Fig.7.2.9). Myofascial release should be considered forthe thigh and patella. Gentle and pain-free stretch-

ing exercises should be done at home on a regularbasis and should address tension in the quadriceps,the upper and lower iliotibial tract, the hamstrings,the hip flexors, the hip abductors, the gastrocnemiusand the soleus. A long-term maintenance program

Vastus lateralis

Vastus medialis

Medial compartment of thigh

Posterior compartment of thigh

Vastus intermedius

Sartorius

Reflected head of rectus femoris

Straight head of rectus femoris

Vastus lateralis

Rectus femoris

Sartorius

Vastus medialis

Quadriceps femoris tendon

Patella

Patellar ligament

Pes anserinus

Sartorius

Vastus lateralis

Vastus intermedius

Rectus femoris

Vastus medialis

Adductor canal

Articularis genus

Suprapatellar bursa

Patellar ligament

Quadriceps femoris tendon

Tibial tuberosity

Attachment ofpes anserinus

Sartorius

Semitendinosus

Gracilis

Figure 7.2.9. Muscles of the thigh functionally and dysfunctionally uniting the pelvis and knee.




should include strengthening in terminal kneeextension in association with isometric exercises ofthe above muscles. Patellar knee sleeves are some-times useful. They might have proprioceptive effectsoffering support. Patients feel less pain and thesupport provides some kind of reassurance.

DYSFUNCTIONS OF THE HIPS

Different terms describe hip dysfunctions. Develop-mental displacement of the hip (DDH) is proposedin replacement for congenital dislocation of thehip to stress the fact that the condition can occurprenatally or postnatally.52 The different variantsof the abnormalities of the hip joint includeshallowness of the acetabulum and capsular laxitywith resultant instability and propensity for disloca-tion. DDH refers to a deficient development of theacetabulum that could lead to subluxation anddislocation.

The femoral head remains well covered by theacetabulum in the early fetal period (between 6 and20 weeks) and dislocation does not occur at thisearly time.53However, at birth, the human acetabu-lum is shallower than at any other time duringdevelopment and is consequently vulnerable for hipinstability.54Mechanical factors seem to play a rolein neonatal hip instability. Moderate loading of thehips at 45 of flexion maintained for 3 hours hasbeen shown to distend the articular capsule and to

produce deformation and dislocation of the jointresembling that found in DDH.55 Modifications inthe pressure on the cartilaginous acetabulum arethought to interfere with normal bone growth.56

Uterine constraint is proposed by numerousauthors as an explanation for the association betweenDDH and other deformations. Foot deformity,57congenital torticollis, congenital postural scolio-sis56,58 and plagiocephaly59are frequently associatedwith DDH. The sleeping position of the infant, witha preference to lie on one side (the side-lying syn-drome), has also been proposed as a contributing

factor to DDH.60Leg postures, associating extension and lateral

rotation, critically predispose the infant to hip dis-location during fetal life and at birth. Interestingly,the newborn psoas muscle is totally relaxed in fullabduction, flexion and lateral rotation. This muscleis always a lateral rotator of the hip, but exerts amuch greater effect when the femur is abducted.61Extending the hip results in a levering action thatis potentially critical if associated with other con-tributing factors such as acetabular or femoral ante-

version and dysplasia.62Caution should, thereforebe exerted when moving the leg into combinedextension and lateral rotation.

DDH occurs in 1 : 1000 live births and is morefrequently encountered on the left side. Beingfemale, first-born

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