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Whiplash Seminar – Concepts for the Practicing Chiropractor

ChiropracticCEWilliam F. Huber, D.C.,

D.A.C.A.N., D.C.B.C.N., M.S. (R)

Whiplash Overview Module

Anatomy, Mechanisms of Injury, and Concepts

Direct Injuries to the Cervical Spine

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Unusual Mechanisms of Injury to the Cervical Spine

More Classic Cervical Spine Injury

Airbags make a Difference!

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Unusual Mechanisms of Car Movement

• To understand the effects of whiplash, more appropriately termed CAD (cervical acceleration/deceleration injury), an understanding and in depth review of the underlying anatomy and its function is essential

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Different Mechanisms of Whiplash

Superficial Back

The superficial layer of the back contains muscles that are innervated by ventral primary rami, and are often injured in motor vehicle accidents that injury the cervical spine. Certain landmarks are utilized in the study of the anatomy of these structures - the most commonly used are the following:

1. mastoid process on the skull2. external occipital protuberance on the skull3. superior nuchal line on the skull4. ligamentum nuchae5. spine of CV7 (vertebra prominens)6. iliac crest on the hip bone7. posterior superior iliac spine on the hip bone

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8. lateral third of clavicle9. scapula

a. vertebral and axillary bordersb. superior and inferior anglesc. acromion processd. spine

Volitional Cranial Trauma

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Skin of the back -A. dorsal skin is thicker than ventral skinB. skin in most areas has preponderance of its collagen

fibers oriented in one direction1. If a round probe penetrates the skin, it will leave a slit-like opening2. Cleavage (Langer’s) lines are parallel to the dominant direction of collagen fibers3. Surgical incisions along cleavage lines tend to leave smaller scars and are less apt to rupture.4. Thus, traumatic lacerations may have a greater or lesser likelihood of complications based on their location and orientation

Spinal Nerves Dermatome: the specific area of skin supplied by a singlespinal nerve

a. named according to the spinal nerve innervating itb. spinal nerve innervation overlap each otherc. not all spinal nerves supply skin on the back

(1) C1 spinal nerve is NOT cutaneous therefore there is NO dermatome pattern for Cl

The area on each side of the dorsal midline is supplied by dorsal primary ramiLower cervical posterior primary rami may not have cutaneous branchesL4 & L5 posterior primary rami do NOT have primary cutaneous branches

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FasciaSuperficial fascia: (panniculus adiposus)

1. fatty layer of connective tissue deep to the skin2. in some areas of the body it may be very thick, but on the back it is usually thin3. distribution of fat in this layer is determined in part by the sex hormones

B. deep fascia1. dense, organized connective tissue sheet that binds together or “invests” the deep structures2. encloses all the structures deep to the superficial fascia3. most prominent deep fascia of the back is thoracolumbar fascia

a. consists of anterior, middle and posterior lamellae and encloses the deep muscles (erectors) of the back

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Vertebrae: CV = cervical; TV = thoracic; LV = lumbar; SV = sacral, CoV = coccygealVertebra parts

1. anterior – body - supports the weight2. posteriorly - vertebral arch - protects the spinal cord

a. paired pedicles - short processes that connect lamina to body b. paired laminae - bone between pedicles and spinous process c. seven processes

(1) spinous process (1)(a) attached in the mid-line where the two laminae meet(b) projects posteriorly

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(2) transverse processes (2,3)(a) paired(b) project laterally from the junction

of the pedicles and laminae(3) superior and inferior articular processes(4-7)

(a) paired(b) project superiorly or inferiorly from the region of the junction of pedicles and laminae, but mostly laminae

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Alteration of CraniovertebralArticulation

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• A recent study also demonstrated a large density of muscle spindle afferents in the longis capitis and longus colli muscles.

• This was especially true of the lateral aspects of the longus colli muscles

• Thus, with injury to these muscles, or the discs and facets, it is possible that the normal feedback mechanisms used to modulate cervical spinal spatial orientation are altered, allowing abnormal movement or correction parameters, that may lead to abnormal bone stresses, or DJD/OA

• These discs also exhibit hysteresis and creep• Creep, the ability to gradually deform under a

constant load, is lost is degenerated discs. • Thus, a pre-existing degenerated cervical

spine will cause the transfer of additional forces to surround tissues when shock or placed under a load

• This may increase injury to surrounding tissue, and be a pre-existing complicating factor to the effects of CAD injury

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• Hysteresis, the loss of energy following repetitive loading and unloading is lost as discs degenerate

• It has also been noted, that degenerating discs, whether caused due to repetitive microtrauma (ie MVA) or pre-existing MVAsexhibit lateral shear (lateral motion) with torsional stresses

• This is believed to produce instability in the disc and results in development of DJD and OA in the uncovertebral and facet joints

• The prior images detail the need for assessment of the patient’s condition prior to the MVA

• Thus, dx alteration is critical for – accurate diagnosis– accurate treatment response expectations– length of active management – home instructions following management– expected long term sequelae– legal and physiologic aspects of each of the above

are dependent on your acquisition of this information

Clinical Interlude

• It is also critical that in the first phases following connective tissue injury, that the proprioceptive function be restored to the joint.

• This is due to disruption of type I, II and III receptors in the connective tissue that tend to be damaged in the “sprain/strain” mechanism

• This will be detailed later

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Proprioceptive Damage?

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• Of interest is that spinal ligaments are uniaxial, designed to carry loads in one direction only

• When stretched an additional 10% of their original length, they fail to return to their original length (more details to follow)

• Their fiber orientation must be in line with the stresses placed on them for them to be effected at combatting the effects of that force

• Soft tissue manipulation (transverse friction massage) has been implicated here

Example of Failed LigamentousIntegrity

• This type of management has been seen to improve the orientation of the collagenous fibers, thus decreasing matting, and increasing strength of injured tissue

• The ALL and PLL have both seen to be ruptured following CAD

• The ALL has been found to be stronger than the PLL in the C spine

• The interspinous ligaments are the weakest in the C spine

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• Ligamentum flava has the greatest density of elastic fibers in the body

• This may allow for reduction in buckling with extension (DJD conditions and myelopathy) as well as to restrict forces of sudden flexion

• This is due to the fact that ligaments strengths increase with the rate of loading

Human Nervous System

• Divided into two anatomical components:– Central Nervous System (CNS) - which

consists of the brain and the spinal cord– Peripheral Nervous System - which

consists of all other neurologic tissue found within the human body

• The functional classifications of the Autonomic nervous system, which has components found in both the CNS and PNS are as follows:– Sympathetic nervous system– Parasympathetic nervous system– Enteric Nervous system

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Peripheral nervous system (PNS) consists of the cranialand spinal nerves, including autonomic nervous system (ANS)

1. 31 pairs of spinal nervesa. 8 cervical (C1-8)b. 12 thoracic (T1-12)c. 5 lumbar (L1-5)d. 5 sacral (S1-5)e. 1 coccygeal (Col)

2. 3rd through 11th thoracic nerves are considered typical; the rest are modifiedWHY ARE THEY NOT CONSIDERED TYPICAL?

Abnormal Nervous Systems

Early Neurologic Development

• In early development a few interesting things occur.

• The body develops in segments, and each segment has it’s own individual nerve supply.

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Typical spinal nerveDorsal (posterior) and ventral (anterior) roots

a. attaches to the spinal cordb. made up of individual nerve fibers/axons which carry nerve impulses in and out of the spinal cordc. nerve fibers/axons are parts of nerve cells or neurons

Dorsal (posterior) root is sensory - afferenta. carries impulses into the spinal cordb. cell bodies of neurons are in the dorsal root ganglionc. distal or peripheral fibers from neurons end in sensory organs or as free endings to pick up sensory stimulid. sensory stimuli are converted to sensory impulses

that are carried from the site of stimulus, through the cell bodies in the ganglion and finally into the spinal cord

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Spinal nerve proper - formed by dorsal and ventral rootsa. contains the sensory and motor fibers from the dorsal and ventral roots

Bell-Magendie Law - still applicable?

Spinal nerve is less than a centimeter in length, it divides into dorsal (posterior) and ventral (anterior) primary rami

Both primary rami contain a mixture of fibers from the dorsal and ventral roots

Dorsal (posterior) primary ramusa. innervates the deep muscles of the back and skin over themb. receives sensory stimuli from all the tissues in the posterior part of the segment to which it belongs

(1) branches into medial and lateral branches, only one of which becomes cutaneous

Ventral (anterior) primary ramusa. passes toward the front of the body supplying muscles

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Reversed Lordosis?

Ventral primary rami may form plexuses- cervical plexus: anterior primary rami of C1-4- brachial plexus: anterior primary rami of C5-T1- lumbar plexus: anterior primary rami of

L1-L4- sacral plexus: anterior primary rami of

L4-S4

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Example of Neurologic Dysfunction

Vertebral Column & Spinal Cord

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• Because of the facet orientation, trauma that has an oblique vector of hyperextension with or without hyperflexion, may cause unilateral facet dislocation

• This is seen as an stair stepping phenomenon on cervical radiographs

• Ligamentous or capsular damage more commonly occurs when these are the vectors of force that the patient suffers

• Thus specifics about head location, location of impact, etc., are critical for tissue evaluation, diagnosis and expected outcome

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• Uncinate processes on the cervical vertebrae and the bodies themselves make up the uncovertebral joints

• These are developed fully by age 18, and are synovial in nature

• They act to limit lateral flexion and extension, and aid in flexion of the cervical spine

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Early Life Trauma

Craniovertebral joints1.atlantooccipital joints

a. articulations between the lateral masses of CV1 and the occipital condyles of the skull b. synovial joints that permit flexion and extension c. anterior and posterior atlantooccipital membranes: connect the margins of the foramen magnum of the skull and the anterior and posterior arches of CV1 d. transverse ligament of the atlas: extend between the lateral masses of CV1 to hold the dens of CV2 against the anterior arch of CV1e. cruciform ligament: formed by bands from the transverse ligament extend to the body of CV2 f. alar ligaments: extend from sides of dens to lateral margin of foramen magnum

(1) check side to side movement of the headg. tectorial ligament: continuation of posterior longitudinal ligament

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• Occiput-atlas articulation allows for 13 degrees of flexion and extension, 8 degrees of lateral bending and no rotation

• Hyperextension here may cause fracture of the posterior ring of the atlas where the vertebral artery crosses the atlas (its weakest point)

• No rotation, but excessive flexion causes the odontoid to contact the foramen magnum (and potentially the cord)

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2. atlantoaxial joints - two lateral and one medial synovialjoints

a. lateral joints - between lateral masses of CV1 and CV2b. medial joint - between dens of CV2 and anterior arch of CV1c.movement – rotation - permits head to turn from side to side

(1)skull and CV1 rotate on CV2 as a unit (2)medial joint is a pivot joint

• Atlanto-axial articulation - 50% of cervical rotation occurs here

• 10 degrees of flexion and extension occur here, and 47 degrees of rotation

• No lateral flexion occurs here

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Cervical Injury Mechanism

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• Zygopophyseal joints may be a source of pain

• Stimulation of these pain receptors causes an increase in activation of local ventral horn cells via intranuncial pools of neurons

• Mechanoreceptors are found in the capsule of zygopophyseal joints, and are – Type I very sensitive static and dynamic that fire

continually– Type II less sensitive the fire during movement– (Additional types to be documented later!)

• These type I and type II receptors have a pain suppressive effect when stimulated

• Additionally, these receptors have a reflexogenic effect that causes a normalization of muscular activity on both sides of the spinal column when stimulated

• This effect is found at the level of stimulation, as well as above and below the level

Proprioception is Critical

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Awesome Proprioception

• This is in addition to the pain suppressive effects via the large diameter afferent path and central descending inhibitory barrages on the nociceptive pathway

• Thus two (higher center mediated and local cord mediated) inhibitory mechanisms to diminish pain via manipulation in the C spine

DJD/OA and Whiplash

• It has been demonstrated the cervical spondylosis within 7 years following CAD occurs at a rate of 39% versus 6% in age matched controls

• With sustained LOCs, this figure is elevated to 60%

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This May Lead to DJD

So Might This!!!

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• Thus, given that statistic, and the common sense approach of mechanical derangement of cervical spinal tissue some issues should become clear - these include:– documentation of pre-existing status - prior injury

to neck – If there is prior injury to the cervical spinal area,

what does this mean?– What should you ask?– What should you expect?– How do you document this?– Does this alter you approach to MMI?

– How do you know where MMI is?– Statements made on narratives -– How would you quantify you diagnosis?– Are these injuries permanent?– Really?– If so, would you release the patient?– If so, what about their permanent injury?– Would you treat the patient in the future as a result

of injuries sustained in this accident - remember you said these injuries are permanent

– Who do you bill for this management?– Who is responsible for this bill?

– Has the case been settled?– Does it matter?– If this is so, what about the patient that you treated

3 years ago for a whiplash injury, and now gets hurt again?

– What if the injury was 15 years ago?– How do you know their current, or past status?– What if they do not return to you prior to the

deposition 1 year later?– Are they still suffering from a permanent injury?– What would you say?

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– Examples• “At this point in time, it appears that based

upon examination findings, response to treatment, and documented healing times of injuries such as these, that this patient has reached the point of maximum medical improvement. However, due to the permanent nature of the injuries sustained, and the defects manifested, the patient is expected to experience continued episodes of soreness and stiffness as well as degenerative changes in the ______ region as a direct result of the injuries sustained in the motor vehicle accident which occurred on ___________. The patient has been given specific advice as to how to handle these epsodes as they occur, and to contact this office in the future for evaluation and management of these episodes if required.”

Muscles of the Superficial and Deep Back related to the

Cervical Spine

• These muscles are divided into layers by most authors. Some authors develop the back muscles in up to 6 distinct layers.

• The focus to follow is on the back muscles that act directly on the cervical spine itself.

• These muscles are mainly extensors• They have been shown to exhibit a

faster stretch reflex than flexors, but require longer to activate

• These are 35% stronger than the flexors• Reflex time in women is 11% faster than

men, but strength is 60% of men

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1. trapezius muscle: a. most superficial muscle of the backb. acts on the shoulder, but not on the shoulder joint, since it does NOT cross the shoulder jointc. innervation: accessory nerve (CN XI) and C3 and C4 nerves

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3. levator scapulae muscle:a. arises from the transverse processes of the

upper four cervical vertebraeb. inserts on the vertebral border of the scapula

above the spinec. elevates the scapulad. innervation: nerves C3, 4 of the cervical plexus and the dorsal scapular nerve (C3,4,5)e. blood supply: dorsal scapular vessels

4. rhomboideus major and minor muscles:a. rhomboideus major: arises below and parallel to the minor

(1) arises from spinous processes of CV7-TV4(2) inserts on the vertebral border of the scapula below the spine

b. rhomboideus minor:(1) arises from the lower part of the ligamentum nuchae

and spine of CV7(2) inserts on the vertebral border of the scapula at the

level of the spinec. innervation: dorsal scapular nerve (both muscles) (C5)d. blood supply: dorsal scapular vesselse. these muscles retract the shoulder by drawing the scapulae towards each other

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D. triangle of auscultation: boundaries include

1. lateral - scapula2. medial - trapezius muscle3. inferior - latissimus dorsi muscle

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Deep Muscles of the Back

A. Deep muscles of the back are located in the vertebral grooves between the anterior and posterior (technically the medial lamellae) lamellae of the thoracolumbar fascia

1. innervation: posterior primary rami of the spinal nerves

2. act on the vertebral column and head

3. splenius capitis: a. origin from the ligamentum nuchae and the

spinous processes of CV7-TV4b. insert below superior nuchal line, mastoid

process, c. action unilaterally - ipsilateral facial rotation, bilaterally extension of cervical spine

d. action of one muscle rotates the head to the same side, also ipsilateral lateral flexion

e. innervation: dorsal primary rami - lateral branches CV3-CV5

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3. splenius cervicis muscles: a. arise from the spinous processes of TV3-TV6b. insert on transverse processes of CV1-CV4c. together they extend the head and neck and

individually turn the headd. action of one muscle ipsilaterally rotates and

laterally flexes the head e. innervation: dorsal primary rami - lateral

branches CV5-CV7

4. erector spinae muscles: aka sacrospinalis musclesa. most powerful deep back muscle and is the

principal extensor of the backb. complex muscle consisting of three columns of

fibers: spinalis, longissimus, and iliocostalis(1) further subdivided regionally

c. innervation: dorsal primary rami - all lateral branches of nearby dorsal primary rami

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Illiocostalis

• Divided into lumborum, thoracis and cervicis divisions

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Illiocostalis Lumborum

• Origin : common origin from thoracolumbar fascia, and spinousprocesses of T11-L5

• Insertion : Angles of lower 6 to 9 ribs• Action : Extends and laterally flexes

spine• Innervation : Lateral branches of dorsal

primary rami of nearby spinal nerves

Illiocostalis Thoracis

• Origin : Angles of lower six ribs• Insertion : Angles of upper six ribs and

transverse process of CV7• Action : Extend and laterally flex the

spine• Innervation : Lateral branch of dorsal

primary rami of nearby spinal nerves

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Illiocostalis Cervicis

• Origin : Angles of third through sixth ribs• Insertion : Posterior tubercles of

transverse processes of CV4-CV6• Action : Extend and laterally flex the

spine• Innervation : Lateral branch of dorsal

primary rami of nearby spinal nerves

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Longissimus

• Divided into thoracis, cervicis, and capitis divisions

Longissimus Thoracis

• Origin : Common origin from thoracolumbarfascia

• Insertion : 3rd through 12th ribs, transverse processes of all thoracic vertebrae

• Action : Extend and laterally flex the spine• Innervation : Lateral branches of dorsal

primary rami of nearby spinal nerves

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Longissimus Cervicis

• Origin : Transverse processes of TV1-TV5

• Insertion : Transverse and articularprocesses of CV2-CV6

• Action : Extend and laterally flex the spine

• Innervation: Lateral branch of dorsal primary rami of nearby spinal nerves

Longissimus Capitis

• Origin : Transverse processes of TV1-TV5, articular processes CV4-CV7

• Insertion : Mastoid process• Action : Extend head, and laterally flex

the spine• Innervation : Lateral branch of dorsal

primary rami of nearby spinal nerves

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Spinalis

• Divided into thoracis, cervicis, and capitis divisions

Spinalis Thoracis

• Origin : Spinous process of TV11-LV2• Insertion : Spinous process of TV1-TV4

(8)• Action : Extend spine• Innervation : Lateral branch of dorsal

primary rami of nearby spinal nerves

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Spinalis Cervicis

• Origin : Spinous processes of TV1-TV6• Insertion : Spinous processes of CV2

(maybe CV3 and CV4)• Action : Extend spine• Innervation : Lateral branches of dorsal

primary rami of nearby spinal nerves

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Spinalis Capitis

• Origin : Transverse process of CV7-TV6, articular process of CV4-CV6

• Insertion : Between superior and inferior nuchal lines

• Action : Extend head• Innervation : Lateral branches of dorsal

primary rami of nearby spinal nerves

5. transversospinal group of muscles:a. semispinalis muscles are the more superficial and extend about 6 segmentsand is the most prominent of transversospinal groupb. multifidus muscles extend 3 to 5 segmentsc. rotator muscles are the deepest and extend 1 or 2 segments

(1) further divided regionallyd. rotation of vertebral column to the opposite sidee. innervation: dorsal primary rami

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B. The suboccipital triangle is a space related to the occipital bone and the first two cervical vertebrae, bounded by muscles and containing the vertebral artery

1. first cervical vertebra or atlas (CV1):a. superior articular facets articulate with the occipital condylesb. vertebral foramen lies immediately below the foramen magnumc. has no bodyd. has a posterior tubercle instead of a spinous process

2. second cervical vertebra or axis (CV2):a. embryological body of the first cervical vertebra is fused to it and is called the odontoid process or dens

3. muscles which bound the triangle are:a. inferior oblique -b. superior oblique -c. rectus capitis posterior minor -d. rectus capitis posterior major -e. innervated by suboccipital nerve, dorsal (posterior) ramus of Clf. as a whole all the muscles extend the head and rotate it and atlas toward the same side

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• When all four muscles contract ipsilaterally, ipsilateral lateral flexion is produced

• This occurs mainly at the atlanto-occipital articulation

• Contralateral inhibition of the entire group occurs

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• Obliquus capitis inferior stabilizes the atlantoaxial joint

• When they contract bilaterally, atlas is extended on axis

• Unilateral contraction causes the atlas to rotate posteriorly on the ipsilateralside

• When all four suboccipital muscle contract the head is laterally flexed to the ipsilateral side - mainly at the atlantooccipital articulation

• Obliquus capitis superior does this most efficiently

Example of the Importance of Proprioceptive Information on

Stability

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• Rectus capitis lateralis also exists, but will be discussed in the prevertebral region

• It is considered a homologue to the intertransverse muscles

• Bilateral contraction flexes the head, and unilateral contraction produces ipsilaterallateral bending

• Rectus capitis anterior is present, and with bilateral contraction, flexion of the skull occurs

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Posterior Triangle of the Neck

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Cutaneous nerves allow us to feel Pain

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One Mechanism of Whiplash

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Arteries to the brain Needed

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Anterior Triangle of the Neck

Divisions of the Anterior Triangle

• Muscular triangle - bordered by anterior border of SCM, superior belly of omohyoid and midline

• Contains the “strap” muscles - properly known as the infrahyoid muscles

• These muscles are named for their origins and insertions and they act on the larynx and the hyoid bone

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Infrahyoid Muscles

• Sternohyoid• Omohyoid• Sternothyroid• Thyrohyoid• All strap muscles are innervated by

branches of the ansa cervicalis

Suprahyoid Muscles

• Act on jaw, mouth and tongue - are innervated by various cranial nerves

• Digastric - anterior and posterior bellies - anterior belly CN V, posterior belly CN VII

• Stylohyoid - CN VII• Mylohyoid - CN V• Hyoglossus - CN XII

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Vessels of the Anterior Triangle

• Branches of the external carotid artery• Facial artery, and it’s submental branch• Accompanied by the facial vein

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Other Important Structures located in the Anterior

Triangle• Mylohyoid nerve - with branches to the

mylohyoid and anterior belly of digastric• Hypoglossal nerve • Lingual nerve• Lingual Artery

External Carotid Artery

• Has numerous branches in the neck– superior thyroid artery (superior laryngeal

br)– lingual artery– facial artery

(submental/glandular/tonsil/palantinebranches)

– ascending pharyngeal branch– occipital branch

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Internal Jugular Vein

• Lies in the carotid sheath• Arises from the intercranial dural

venous sinuses• also receives common facial vein

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Cranial Nerves found in the Cervical Spine

• Trigeminal - supplies anterior belly of digrastic and mylohyoid

• Facial - supplies posterior belly of digastric as well as platysma

• Glossopharyngeal - supplies the carotid sinus

Vagus Nerve

• Supplies heart via superior and inferior cervical cardiac nerves

• Superior laryngeal branch supplies cricothyroid muscle as well as sensory to larynx, and also other branches - the most important of which is the recurrent laryngeal nerve, which supplies the vocal folds

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The vagus controls gut function

The vagus controls gut function

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Cranial Nerves (cont)

• Spinal Accessory - enters deep surface of the SCM to supply it

• Hypoglossal - crosses external to carotids

Ansa Cervicalis

• Cervical Plexus of nerves• Formed from C1-C4 ventral primary

rami• Innervate strap muscles• Found anterior to internal jugular near

the cervical and hypoglossal nerves

Thyroid Gland

• Two lateral lobes that are found from oblique line of thyroid gland down to the level of 6th tracheal ring

• Has extensive blood supply via the superior and inferior thyroid arteries

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Prevertebral Region

• An existing space which is posterior to the pharynx, however, is anterior to the vertebral column. Certain muscular groups reside in the prevertebral region (4mm space width @ C3 and injuries)

• Seven to be exact - The three scalene muscles, longus capitis, longus colli, rectus capitis anterior and rectus capitis lateralis

• The scalene muscles - already described

• The longus colli and longus capitis are to be covered here - both are found on the anterior aspect of the spinal column, and both act to flex the cervical spine and head respectively

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Longus Colli

• Originates from the anterior tubercles of TPs of C3-5 and inserts on anterior tubercle of C1

• This muscle acts to flex the act as well as aid in ipsilateral lateral bending, and is innervated by local ventral primary rami

Longus Capitis

• This muscle arises from the anterior tubercles of the TPs of C3-6, and inserts on the anterior portion of the occiput.

• It’s action is flexion of the head, and it is innervated by ventral primary rami of C1-3

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Rectus Capitis Anterior

• Origin from anterior portion of lateral mass of atlas, and inserts on the occiput, anterior to occipital condyle

• Acts to flex the head at the atlanto-occipital joint, and is innervated by C1/2 ventral primary rami

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Rectus Capitis Lateralis

• Origin: Anterior aspect of TP of C1, and inserts on the occiput. Thus this muscle provides for lateral flexion of occiput on atlas.

• Innervated by the ventral primary ramiof C1/2.

Pharynx

• In effect, the pharynx is a muscular tube • It is the open region at the posterior

portion of the nasal and oral cavity, and has three parts - nasopharynx, oropharynx and laryngopharynx.

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Basic Kinematics for the C Spine

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Deceleration Mechanisms

Lateral Flexion Mechanisms

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Notice Multiple Vectors of Injury

• In the cervical spine, coupled motion occurs• This means that rotation is always

accompanied by lateral flexion and vice versa• Normally, with right lateral flexion, the

vertebral bodies rotate into the concavity, allowing for spinous rotation in the convexity of the laterally flexed C spine

Current Thoughts on Whiplash Injury

• Currently, a common misconception is that low speed impacts cannot produce injuries in the car occupants.

• The change in velocity can be an indicator of amount of kinetic energy imparted during a motor vehicle accident

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• Because of this low speed - no injury concept, this area of investigation and protection has been neglected.

• This is now changing, with current investigations taking place with low speed impacts, with human volunteers

• Thus, more accurate evaluations of the actual events are occurring

• Below 30 mph, there are no Federal Motor Vehicle Safety Standards crash test requirements.

• Also, there are no established neck injury criteria, and no occupant safety-related lower crash worthiness requirements.

• This adds to the often misunderstood nature of cervical spinal injuries that occur as a result of low speed impacts.

• This thought process does not include the following:

• If a vehicle is significantly deformed, that indicates that the force of the impact was transferred and absorbed by the vehicle itself

• Thus, less energy is available, as it has been absorbed the by destruction of the vehicle itself

• This is the explanation for “disintegrating”vehicles in professional racing

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Motor Vehicular Damage

• For example, at a 8.5 mph rear end impact, the shoulder of the occupant experienced 8 g of force, while the vehicle itself experienced 5.5 g of force

• The g force on the occupant is greater than that on the vehicle, and if vehicle damage is less, the occupant absorbs more accelerating forces

• The study showed that vehicle damage became apparent at 8.7 mph damage

• What this indicates is that the occupant of the vehicle absorbs forces that are greater than what is imparted to the vehicle itself

• Additionally, the greatest increases in occupant acceleration occur before visible damage to the vehicle occurs

• This is important to be aware of to prevent the concept of vehicle damage and repair costs being directly related or proportional to the amount of injury in a patient

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More Facts

• Rear impact MVA’s are the vector of force that produces cervical spinal injury most frequently.

• This is a biphasic injury, with a component of extension and flexion.

• The frontal impact is monophasic with only a flexion component.

• Although the posterior muscles are of greater clinical significance.

• The patient’s pre-existing status is important for evaluation of likelihood and permanence of injury

• Increased age = decreased mobility, with increased DJD, and decreased elasticity, decreased reflex time, strength decreases

• Shorter occupants suffer less injuries, but female drivers tend to suffer greater amounts of injuries, as well as more serious injuries, and prolonged symptoms and disability

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• Interesting data –– From Spine Volume 29, #11, pp 1217-1225– 50% of CAD pts reported chronic cervicalgia 15

years post MVA– C spine disc injuries have been consistently

documented via radipgraphs in MVA patients– 25% of patients had cervical herniated disks likely

from CAD– 20% of whiplash pts had severe disc herniation

correlated with radicular symptoms

– Cartilaginous endplate injuries and disc herniationare seen following CAD

– Higher incidence of DJD follow CAD– 39% of whiplash patients had DJD 10 years post

MVA when no signs of DJD found at time of injury– Incidence of CAD twice that in groups of patients

that required fusion – Also, this study demonstrated the effects of the

fibers of the disc as well as the disc itself to loads from CAD

– It appears that vast majority of injury occurs at the peak of posterior accelation, and entering into the flexion component of a two component injury

– These findings indicated that physiologic limits were exceeded at 3.5 g of stimulation at C4/5

– At 5 g these spread to C3/4, C5/6, and C6/7– The highest strains occur in the posterior fibers– Posterior fiber strain developed to as high as

51.4% in C5/6 posterior area at 8 g of stimuli– % dropped from here with greater stimuli– Disc shear strain occurred from posterior

translation at C5/6 during 8 g of stimuli– Both fiber and disc shear strain were highest in

posterior disc region– It was discovered that a rear end CAD can injure

the disc anteriorly via elongation, but posteriorlydue to these shear forces

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– It was determined that with low impact accelerations (25-35% strain at 3.5 g of force) that C4/5 and C5/6 discs were at risk for failure

– Also, at higher accelerations the C3/4 and C6/7 areas were at risk of injury

– This data is interesting when coupled with the study by Severy from the Canadian Services Medical Journal11:727 1955, that states that the head acceleration of an individual in a 8.5 mph rear impact was 10 g

– Also noted in this study was that the car suffered 5.5 g of force, the shoulder 8 g of force and the head 10 g of force

– Thus, the patient experiences more g for than the vehicle with low impact injury, or a force several times greater than suffered by the vehicle itself

– A study by Thomson RW in a report “Energy attenuation within the vehicle during low speed collisions, 1989 indicated that increasing head and shoulder acceleration occuring and increased until about 9 miles per hour, at which time these acceleratory curve flattened out (peaked)

– Also he noted that visible damage to the vehicle occurred at 8.7mph, after the largest amount of acceleration had occurred to the occupant!

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• These findings were also verified and described by Romilly, DP in Proceedings of the 12th International Conference of Experimental Safety Vehicles in Gothernburg, May 1989;1-4

• Severy also described these force in Automobile barrier and rear end collision performance – this paper presented at the Society of Automotive Engineers Summer meeting, Atlantic City, NJ, June 8-13, 1958

• Irish Medical Journal – 2003, Feb;96(2):53-4 “Chronic neck pain following road traffic…”– This study demonstrated that the mean

duration of neck pain following MVA was 15.5 months, with a 90% seatbelt use

– Mean off work time was 4.9 months, with 60% also reporting low back pain

• JMPT– 2002, Nov-Dec;25(9)550-555– This study demonstrated that the whiplash group

of patients studied demonstrated a significantly increased amount of flexion at the C4/5 region compared to asymptomatic patients

– Thus, an altered cervical lordosis is noted following MVA, especially at this level, although overall global appearance may be normal

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• “Evidence for Spinal Cord Hypersensitivity in chronic pain after whiplash and in Fibromyalgia” – Pain, 107 (2004) 7-15– This study demonstrates that following MVA and

in fibromyalgia patients, there is an increase of hyperexcitablity of the spinal cord. These patients demonstrated painful responses to usually non noxious stimuli, via altered motor output, and in the absence of apparent tissue damage

• Journal of Whiplash and Related Disorders –Vol 2(1) 2003– Chronic Pain after Whiplash Injury – Evidence for

altered Central Sensory Processing• This study also stated that it appears that nociceptive

stimuli, from an unknown source, irreversible changes in the nociceptive system, pre-injury altered sensory processing and psychologic factors may all contribute to hyperexcitability of the spinal cord following MVA

Unusual Mechanisms

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• Quantitative studies of chronic faciliitation in human motoneuron pools – 1947 – Denslow, Korr, Krems– This study states that motor neurons are at a

resting state not close to threshold, or any volley of incoming dorsal horn signals would cause a reflexive response

– This is a toning down response – However, in a “normal” individual it was noted that

this can not be the case as • Certain pools of neurons close to each other can be at

different threshold levels• Some neuronal pools can be at or above the threshold

level, without external stimuli

– It was seen that some segments of the cord were at a low threshold level, others at a slightly higher threshold, and others at even a higher threshold

– This reflects a “central facilitation,” and this facilitation shows a hyper excitability to local and distance stimulation

– Thus, impulses can enter, bypass a higher threshold segment, and be seen to effect a distal low threshold segment – usually the spread is from high to low threshold segments

– Columns of homologues neurons– All of these occur in “normal” humans– These were tested with response of muscles to

spinous process pressures

• This central facilitation was also seen to correlate with– Reflex threshold– Palpable supraspinous tissues– Lower levels of pain perception– Also, lasting soreness in these tissues

following minor trauma

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– These differences were seen segment to segment, and patient to patient

– This differences can be present for months– It appears that the chronic segmental

facilitation is dependent upon the facilitating impulses arising from segmentally related structures

– Could these be spinal related structures?

• Korr and Goldstein – 1948 – Dermatomalautonomic activity in relation to segmental motor reflex threshold– These pools of motor neurons are kept at a

chronic facilitated state due to chronic bombardment of impulses from segmentallyrelated structures

– This facilitation is seen here to extend to the IML, as measured in SNS vasomotor activity, as sweat gland activity is related to motor activity

– These differences were found most reliably next to the spine

– These segments are found to often be hyperesthetic, and exhibit the characteristics of trigger areas

• “Skin resistance patterns associated visceral disease” – 1949– Reported patterns between visceral disease and

electrical skin resistance– Segmental relation to low resistance segments

and viscera were established– These were also consistent with disease

processes and segmental levels and referred pain patterns

– Also seen was the presence of these segmental differences over areas prior to the clinical onset of the underlying visceral disease

– The lowest resistance levels corresponded to the most sensitive regions of these zones

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• Also, studies from osteopathic institutions in the 1920’s reveal– That there is correlation with vertebral levels and

visceral disease– That when the spine was immobilized, visceral

disease was seen to develop in the tissue of the viscera

– When the immobilization was reversed, the overt pathology was reversed, however, cellular differences of the pathology could still be noted

• Patterns of electrical skin resistance in Man”– 1958 – Korr, Thomas, Wright– Interruption or retardation of flow of sympathetic

impulses to an area of skin causes marked elevation of resistance whether this is due to multiple different sources

– The opposite of this is true as well– This is found in normal individuals– Present for long periods of time – in some

individuals for a period of 2 ½ years!– Other areas may be absent from time to time– Some of these low resistance areas are truly

dermatomal indicating a segmental origin– Confusion with radiculopathy? – MS? – etc.– Also, this sympathetic alteration can occur from

trauma, surgery, pain syndromes, visceral disease, cord disease, etc.

• Effects of experimental myofascial insults on cutaneous patterns of sympathetic activity in man” –1962 – Korr, Wright, Thomas– This study was designed to investigate the effects

on the SNS with myofascial irritation• Injection of hypertonic saline into areas resulted in areas

of lower resistance• These following anterior peripheralization patterns

following injection• Pelvic tilt stools were also used that demonstrated

changes in lower cervical, lumbar and thoracic (lower) regions

• However, the distribution and amount of change varied from person to person

• These differences were also noted to almost completely reverse in some individuals after 30 minutes following rectification

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– Heel lifts that were placed in shoes had the effect of developing pai in the lumbosacral region, and associated low resistance areas

– This was seen in some to progress with a day interval to extend to the mid thoracic region –interestingly enough, the lift was removed

– After removal, the areas of low resistance were continue to be noted in the mid thoracic area at his last evaluation – 16 months after the lift was removed

– This appears to be the pattern – persistant lower resistance areas following their initiation – being worse with activity as the day progresses

– This also was seen with the removal of a therapeutic lift

– Following removal, areas of lower resistance developed and pain returned

– Also noted, is the fact that visceral , circulatory, and thermoregulatory functions are controlled by the ans, and are continually coupled in organized patterns to musculoskeletal activity

– Efferent activity in neuromuscular and ANS pathways is functionally coordinated by the CNS

– More importantly, it is noted that efferent components of patterns of motoneurons and preganglionic autonomic neurons are multisegmental and under the bulbar, diencephalicand cortical centers – however, their activity is continually influenced by afferent impulses that arise in thermal receptors, pressure receptors, proprioceptors, pain endings, etc. – all entering the cord via the dorsal horns

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– This means that influences of the mechanoreceptors and pressure receptors, and proprioceptors influence this acitivity

– Additionally, this paper states that the afferent information that enters via the dorsal roots (often painful), become so dominant that they supercede the vertically organized patterns that are ordinarily active, and disrupt them.

– These are not a functional adapation, but an abnormal response, and tend to persist after the influence is removed

– Also irritation in tissues tend to demonstrate changes in the cord segment of innervation of the tissue

– Possible origin of RSDS

– Also, it has been seen that autonomic changes, such as pain, tenderness, spasm, etc., often accompnay visceral disturbances

– The impusles dominating the segmental pathways originate in injured, ischemic, distended or irritated internal organs,

– Their sensory fibers, usually traveling with sympathetic paths, enter the cord

– So, somatic and autonomic patterns are similar– In addition, lower resistance areas and of

vasoconstriction or dilation are parts of reflex responses to streams of impulses originating in somatic and visceral structures, or perhaps the nerve fibers irritated by them

– Also suggested is the fact that the continued hyperactivity of the efferent neurons may be due to a chronically augmented irritability of central neurons

• Sustained Sympathicotoinia as a factor in disease – 1978 –– This paper discussed the fact that “chronic

hyperactivity of SNS seems to be a prevailing theme in many clinical conditions”

– The clinical manifestations are determined by the organs or tissues which are innervated by the hyperactive neurons (although vasoconstriction is a common theme seen at the end organ)

– For the SNS to function normally, it must receive directly, via segmental afferent paths, and indirectly, through higher centers, sensory input from the musculoskeletal system

– It effects on different target tissues are described

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Innocuous mechanical Stimulation of the neck and

alteration – Auton. Neuroscience 2001 August

• Authentic manipulation of C spine was compared with sham manipulation to judge the effects on heart rate

• C1 and C2 were the sites of influence• DCs performed manipulation of the subjects,

rotary adjustments with audible release• Sham adjustments involved set up, no thrust,

no audible release• A reduction in heart rate in the first five

minutes was shown in only the adjustment group, indicating SNS inhibition

• This is believe to be secondary to mechanical afferent input from receptors in the cervical spine

• Also seen to alter BP

• As stated previously, sympathatocoinia is linked to the following disorders:– Neurogenic pulmonary edema – with increases in

sympathetic activity, edema, changes in capillary permeability, etc. have been seen

– Peptic ulcers and pancreatitis – it has been shown that mild, non lethal bile induced pancreatitis can be converted to hemorrhagic necrotizing and lethal forms via sympathetic stimulation. If ischemia occurs (sympathacotoinia), mixing of bile and pancreatic juices produced parenchymalnecrosis developed – when no ischemia was present, only non necrotic changes were seen. Additionally, the disorders could be seen with ischemia alone – cause?

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• Sympathatocoinia – in splanchnic nerves, this was seen to favor arteriorsclerotic lesions.

• HTN – an increase in splachnic fiber frequency of firing seen in this condition

• Heart Disease – elevated SNS signals may be a factor in heart disease– Decreases in SNS firing from the stellate ganglion

were seen to protect the heart against ectopicdischarges and arryhythmias that are produced by coronary ischemia

– However, increased SNS activity lowers the fibrillation potential – also this is thought to be the mechanism by which postinfarction ectopic activity and arrhythmia develop

– Reduction of SNS activity lowers the mortality rate and complication rate of these factors

• If left SNS activity lowered, a decrease in fibrillation threshold of 72%, right side of 48%.

• Left sided decreased SNS has been suggested for reduction of arrhythmias (ie, for left sided AV node conduction issues, and thus left hemispheric stimulation or descending modulatory regulation via SMT.

• These findings seen to be at the segmental levels (T1-3), and it has been shown that an increase in the SNS activity in these regions may lead to severe cardiac lesions

• It also has been found that increased retention of sodium and water in CHF are ascribable to increased SNS activity in the kidneys

• Facilitated segments on the ipsilateral side of renal function, when overlayed with emotional stress, can reduce the GFR and renal perfusion

• Posttraumatic pain syndromes- RSDS or regional complex pain syndrome manifestions– initial red, swollen area, with subsequent vasospasm, ischemia, Raynaud response, paresthetic impulses, immobile limb position, trophic changes in skin, thinning, loss of hair, shortened tendons, atrophy, osteoperosis, etc.

• Small magnitude injuries produce excitable internuncial pool neurons, with sensory, motor and sympathetic output changes

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Conceptual Summary

• Increased or “facilitated” region of the cord - C versus A delta

• Hyperesthetic vs Hypoesthetic symptom• Increased cord level activation of SNS• Effects of large amounts of

neurtransmitter in the cord and the periphery

• Increased bombardment of intermediolateralcell column, and alpha and gamma motor neuronal pools

• Increased local motor tone• Reduction in local motion• Reduction in cortical activation• End organ pathologic changes with telomere

considerations• Mitotic division rates

• Interesting Info -– Adrenals (considered ganglia of SNS) secrete

epinephrine and norepinephrine– Each has Alpha and Beta sub types– Receptors have specific binding sites -

• for example, in the lungs, to dilate the bronchioles, epinephrine would be used

• Mucous secretion from chronic stimulation• These chemicals have inflammatory

properties in large amounts at the end organ site

• Chronic stimulation can generate long term C fiber activation, and further enhancement of the “wind up” at the neurologic level

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• During states of increased tension or anxiety, the locus coeruleus of the bainis constantly active

• This area is a controller in the sympathetic nervous system

• This is considered by some authors to be a predominant finding in some chronic pain and disease states

• Inflammation -– seen to follow immobilization of joints in an

animal within 4 days– characterized with fibrosis, angiogenesis

and WBC (lymphocyte infiltration)– Intra-articular adhesions have also been

noted

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Hypomobility and it’s effects

• Research has shown that animals with experimentally subluxated levels of the spine demonstrate pathology in the tissue levels of the viscera in a segmental fashion

• These could be stopped or reversed when the subluxation was reversed

• Evidence still present microscopically

• Immobilization of a joint -– Believed to decrease firing of Type I and Type II

facet mechanoreceptors– This allows for increased nociceptive firing in the

cord– Thus an increase in gamma and alpha motor

neuronal activity, and reduced segmental motion– Inflammation or immobilization of a joint for a

period of several weeks destroys these mechanoreceptors permanently

– Local and central consequences and rectification

• Effects of the subluxation complex on the viscera can now be theorized

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• Journal of Electromyography and Kinesiology – Volume 12, Issue 3 June 2003

• This study demonstrated the following– The capsule, disk, ligaments were all innervated

with abundant afferents that were capable of monitoring proprioceptive and kinesthetic information

– Mechanical stimulation of more than one of these viscoelastic tissues results in more excitation of local musculature

– Overall, it seems that spinal structures are well suited to monitor sensory information as well as control spinal muscles and probably also provide kinesthetic perception to the sensory cortex

– Lesions and inflammation in the avascularsupporting structures of the spine and SI joints will disturb the proprioception function of the different receptors and result in increased and prolongeedmuscle activation that may cause pain

– Stimulation of the disc annulus fibrosus induced responses in the multifidus on multiple levels and on the contralateral side, whereas stimulation of the z joint capsule induced reactions predominantly on the same side and segmental level as the stimulation – thus disc injuries may cause bilateral decreases in motion, where facet inflammation may cause ipsilateral reduced motion

– The mechanically induced stretch reflex of the Z joint resulted in reduced motor activity

– Thus the z joints are seen to have a regulatory function, controlling the intricate neuromuscular balance of the motion segment

– Normal locomotion and posture require multiple levels of neural control

– Descending signals from the brainstem activate complex reflex systems in the spinal cord where the myotatic units with their receptors and polysynaptic circuits are the building blocks

– Afferent information is essential in the modification of muscle activation to make it well coordinated and functional

– Mechanoreceptive responses to normal loading and movements probably have a primary effect on modulatioin and modification of descending signals

– ie. That means that the mechanoreceptors drive higher brain function.

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• Injury, certain mechanical loading patterns, degenerative processes and or inflammation may cause perturbation in the proprioceptivefunction of different receptors and result in increased or prolonged muscle activation by triggering reflex activation of the involved muscle groups, which over time can cause pain.

• Spinal ligaments are associated with complex proprioceptive sensory inputs from nearby discs and capsules

• Compared to other joints, the spinal motion segment has more innervation and is more complex, consisting of an intervertebral disc and two z joints

– Normal locomotion requires multiple levels of neural control. To support the body against gravity, maintain posture and to propel it forward, the nervous system must be able to coordinate muscle contractions at many joints. At the same time, the nervous system must exert active control to maintain balance of the moving body, and it must adapt the locomotion pattern to the environment and to the overall behavioral goals. The spinal circuits activated by descending signals from higher centers accomplish this. Neural circuits in the cord play an essential role in motor coordination. Spinal reflexes where the myotaticunits are the building blocks, provide the nervous system with a set of elementary patterns of coordinaton that can be activated, either by sensory stimuli or descending signal from the brain stem and cerebral cortex.

Muscle spindles and GTOs provide proprioceptive information essential for controlling muscle tone , thereby joint stablity.- the neurological feedback from passive viscoelastic structures provide sensory information needed to regulate muscle tension and hence the stability in the spine

The functioning of the motor system is intimately related to that of the sensory system

The proper moment to moment functioning of the motor system depends on a continuous inflow of sensory information

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– Sensory information influences motor output in many ways and at all levels of the motor system

– Motor reflex responses and programmed voluntary respones are dependent upon spinal cord sensory input

– The nerve endings in the outer annulus of the disc, the capsule of z joints and in the ligaments are most likely part of a proprioceptive system responsible for optimal recruitment of the paraspinal muscles

– Mechanoreceptors are thought to play an important role in the function of monitoring position and movements of joints by regulating and modifying muscle tension

– Descending signals that initiate muscle action are modified by the sensory input from the proprioceptive nerve endings

– Overload forces on specific parts can be detected by proper functioning joint sensory receptors and inhibit the involved muscles and thereby prevent injury

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• Damage done to ligaments and perhaps other passive structures does not necessarily have to result in a lot of pain, but it can still result in inappropriate muscle activation

• Stimulation of the outer annulus of disc, z joint, cause activation of paraspinalmusculature, on the same level as well as different levels

• This interaction stabilizes the segments to each other and helps maintain posture

– A lesion in one location may cause alteratioins in muscle activation in other than the actual segment and also on the contralateral side

– The afferent input from sacroilliac joint receptors, as well as mechanoreceptors in the disc and z joint will contribute to different degrees of the muscle activation and may constitute an integral regulatory system

• Change in length and loading of the ligmaents may result in altered firing patterns and changes in the coordination pattern of the muscles

• Decreased interdiscal space from DJD causes less efficient adaptation of the surround nerve endings causing less optimal neuromuscular reflexes

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Sensory Function of Ligaments – Journal of electromyograpohy and Kinesiology Volume 12,

Issue3, June 2002– The ligaments of every joint provide such a

complex sensory feedback mechanism further fortifying the fact that feedback from ligaments is an integral part of joint motion

– The coordination of muscle function around joints and joint movement is influenced by many factors these include:

– Afferents from ligaments, muscles, tendons, skin, vision, etc.

– All of these inputs are mixed with earlier experience stored in the cortex and cerebellum, and these inputs are used to update or change the pre-programmed motor functions which secure an optimal coordination of muscle function in relation to the desired motor activity

– The effects of the sensory system inputs are modified, dependent on ongoing activity in all parts of the system

Spine 1997, Jan1;22(1):17-25– Stretching a single spinal ligament produces a

barrage of sensory feedback from several levels of the cord, on both sides

– This was seen in the dorsal root ganglia, the intermediate gray matter of the cord at the level of stimulation as well as levls above and below the site of stimulation

– This was greater ipsi than contra, but also seen in the sympathetic ganglia at these sites

– Activation was seen also in the dorsal column nuclei, as well as in the vestibular nuclei and thalamus

– It appears that this information was relayed via the dorsal column system and the spinocerebellarsystem

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• ACTA Biol Hung 2002;53(1-2:229-244– SNS regulates cytokine production– All lymphoid organs primary and secondary

and other tissues are involved in immune responses and are heaviliy infuenced by NA derived from varicose axon terminals of the SN

– Circulating catecholamins are also able to influence immune responses, the production of anti-inflammatory and pro inflammatory cytokines by different immune cells

– These are mainly governed by the hypothalamic/pituitary axis

– Under stressful situations the NA released from sympathtetic terminals was able to inhibit the production of proinflammatoryctokines, and increase antiinflammatorycytokines

– Annals of internal medicine, volume 136, No. 10, pages 713-722

• This study demonstrates effectiveness of 6 weeks of treatment for nonspecific neck pain

• Results demonstrated that there was a 68% resolution for manual therapy group, compared with 51% for PT patients and 36% for continued physican care patients (manipulation was 1X/week, PT 2X/week

• 1988 American Journal of Anatomy– Mechanoreceptors in articular tissues

• Most of the receptors in ligaments are found in it’s distal portion

• Concentration of mechanoreceptors appears greater in areas related to the extremes of movement and probably represents the first line of defense in sensing these extremes

• Discharges from these, spindles, and joint mechanoreceptors are thought to function in alerting the CNS of impending injury, and thus averteing this type of injury

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• Journal of Elec. And Kinesiology –June 2002– Theoretical and experimental evidence indicated

that ligament afferents, with afferents ffrommuscles and skin provide CNS with info on movment and posture through ensemblecodingmechanisms, rather than via modality specific pathways. These are triggered when the ligament is threatened by potentially harmful loads has been questioned, and is seems more likely that these sensory inputs participate in continuous control of muscle activity via feed forward mechanisms, and therefore are important in joint stability, reflex regulation, and muscle function by contributing to muscle stiffness through reflex modulation of the gamma muscle spindle system.

• Anesthesiology –1994, Feb. Lanter, et. Al – “The cerebral and systemic effects of

movement…• This study demonstrated cerebral activation as

well as vasodilation in response to muscle spindle afferent activation. These animals demonstrated increased EEG activity subsequent to muscle spindle activation, as well as cerebral vasodilation that was in excess to the metabolic demands of the requirements of the brain.

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• Brain 1991 – March – “Cerebral Potentials…”– This study demonstrated that muscle

spindle and other afferents from movement can be demonstrated by scalp electrodes in the brain.

• Spine – 1994, March McLain, RF– This study demonstrated the distribution of

mechanoreceptors in synovial joints, and lists the types of receptor identified. The density seen in the cervical spine was seen to be the greatest of spinal regions, and dense at C5/6 and upper C spine, as well as indicating that these were responsible for informing the CNS of activity in these areas proprioceptively.

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• Spine 1995 – Nov. (Pickar JG)– This study demonstrated that majority of

endings found in facet joints were graded responses. Additionally that this graded response increased relative to the direction of force applied. Thus the mechanosensitive ending in the spinal joints show direction specificity to facet manipulation. This indicates the benefit of specific adjusting, not global movements.

• Neuroimaging – 2004, August Volume 22 –Issue 4 pages 1722-1731– This study demonstrated that posture and gait

(motor phenomenon) are involved with peripheral, spinal, and supraspinal structures. Separate and distinct activation and deactivations were seen in patterns with BRAIN IMAGERY. Standing imagery activated the thalamus, BG and cerebellar vermis, walking activated the parahippocampal and fusiform gyrus, occipital visual area and cerebellum and running imagery predominantly activated the cerebellum in vermisand adjacent hemisphere. Deactivations were seen in walking and running in the vestibular region. Automated locomotion like running is seen to be based on spinal generators of sensation whose pace is driven by the cerebellar locomotorregion.

Low Speed Impacts - MVAs

• Often described as a change in velocity is 10 mph or less

• Spinal cord injuries have been known to occur in impacts of under 20 mph, and injuries occur, especially where ejection or partial ejection from the vehicle occur.

• Clinical consideration of age, gender, stature, pre-existing injuries and medical considerations is critical for evaluation.

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Classifications of Severity of Whiplash Associated

Disorders• Two scales will be considered here

– The Quebec Task Force Grading System -published in 1995

– The Croft CAD Classification System -published in 1992

Quebec Task Force Grading System

• Grade 0 - No neck complaints; no physical signs

• Grade I - Neck pain, stiffness, or tenderness only; no physical signs

• Grade II - Neck complaint and musculoskeletal sign(s) (these signs include decreased ROM and point tenderness)

Quebec Task Force (cont.)

• Grade III - Neck complaint and neurological sign(s) - (neurological signs include decreased or absent DTRs, weakness, and sensory deficits)

• Grade IV - Neck complaint and fracture or dislocation

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Recent Study• A study in European Spine Journal of June

2003, revealed that the Quebec Task Force grade for patients with pre-existing damage of cervical spine or pre-existing signs differed significantly from those patient without that history.

• What this indicates is that a grade based on the QTF is cannot alone explain the symptoms unless the individual relevant biomechanical factors are considered.

• In fact, in 50% of cases where the technical analysis was performed alone without considering patient history and collision circumstances, the symptoms could not be explained by the impact alone.

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Croft CAD Classification System

• This includes three (3) different grading criteria;– Type of Collision– Clinical Presentation– Stages of Recovery

Type of Collision

• Type I - Primary rear impact• Type II - Primary side impact• Type III - Primary frontal impact

Clinical Presentation

• Grade I - Minimal: no limitation of motion; no ligamentous injury or neurological findings

• Grade II - Slight: limitation of ROM; no ligamentous or neurological findings (these neurological findings can include subjective complaints such as numbness, tingling, etc.)

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• Grade III - Moderate: limitation of motion; some ligamentous injury; neurological findings may be present

• Grade IV - Moderate to severe: limitation of motion; some ligamentous instabilitiy, neurological findings present; fracture of disc derangement (fracture can include minimal end plate fx, disc derangement can include non-herniated forms)

• Grade V - Severe: requires surgical intervention (this seems to be consistent with levels of soft tissue injuries graded elsewhere - such as mild/moderate/severe - these often have healing times referred to as being 6-8 weeks, 14-22 weeks, and requiring surgical intervention respectively)

Stages of Recovery

• Stage I - Acute: inflammatory stage (up to 72 hours)

• Stage II - Subacute: repair stage (72 hours to 14 weeks)

• Stage III - Remodeling stage - (14 weeks to 12 months or more)

• Stage IV - Chronic: Permanent

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• Note - The duration of stage is dependent uon the severity of the initial injury and other factors

• These factors include pre-existing injuries, orthopedic problems, disorders that impact connective tissue formation, would healing times, lifestyle, etc., and must be included as complicating or limiting factors associated with the diagnosis

Additional Information

• The majority of injuries that occur in rear impact MVAs occur at or below a 10 mph change in velocity

• Also, the use of restraints is an important factor in all vector injuries

• With changes in velocity of 16 mph, 50% of the cumulative serious injuries have occurred

• By a change of velocity of 25 mph, 50% of cumulative fatalities have occurred

• Also, with side impact injuries, often the change in velocity of the occupant exceeds that of the vehicle, so a direct correlation of injuries and velocity changes cannot be made accurately

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• The onset of symptoms following MVA is often delayed.

• The mean onset of symptoms following injury is reported to be 72 hours.

• Also, as reported these cervical spinal injuries, many of the patients never fully recover symptomatically - and this must be considered in association with active management strategies

Specifics Regarding Soft Tissue Response to Injuries

• Broken into multiple stages• Each to be described separately

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• Acute Inflammatory Stage - seen to have the cardinal signs of inflammation– redness– swelling– heat– pain– This lasts from 24 to 72 hours– The following occur -

• Capillary walls leak, and leukocytes invade secondary to chemotactic agents via diapedesis

• Monocytes enter, and are transformed into macrophages

• Macrophages phagocytose debri and produce collagenase and other enzymes to degrade ECM and tissues

• Macrophages also attract fibroblasts via fibronectin release

• Macrophages release angiogenic factor• Platelets release growth factor to promote

mitosis of fibroblasts• Fibrotic repair is dependent on the

macrophage - so antiinflammatory meds (steriods/aspirin) may suppress motility of WBCs, and therefore may not be beneficial for the long term recovery of the tissue

• Mast cells release histamine, and seretonin is released by mast cells and platelets

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• Histamine is a vasodilator, and serotonin acts to increase fibroblastic proliferation and collagenous cross-linking activity

• Cell membrane damage causes release of phospolipid (the main constituent of cell walls), and this gets converted to luekotrienes, cyclic endoperoxides, prostacyclin, prostaglandins and thromboxane

• These are pain promoters, vasoconstrictors, and vasodilators

• Anything that alters or interferes with this conversion, may reduce pain or inflammatory processes

• Vitamin C has been shown to inhibit one of these conversions, thus limiting the inflammatory response (potentially)

• Other antiinflammatory meds act on this cascade of conversions to limit the inflammatory process that is seen secondary to capillary exudate from increased local circulation and permeability

• Hyaluronic acid also is released by mast cells • The inflammatory fluid is rich in fibrinogen,

and will develop into collagenous scar tissue• Thus excessive inflammation may lead to

excess collagen, and “matting” of connective tissue, with eventual retraction of the tissue forming a restricted matted scar in the injured area

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• Control of inflammatory process, without eliminating it, is critical to the repair and recovery of the injury

• Also, tissues at this stage are predisposed to hemorrhage, so aggressive STM or SMT or exercise are contraindicated

• STM may aid in venous flow of blood, may allow movement of macrophages, which would reduce chronic inflammation, and potentially scar tissue formation/retraction

• US has also been shown to decrease the inflammatory process

• Heat may increase bleeding, and thus may increase inflammation and potential scar formation

• Fibroblasts are stimulated to enter the area by macrophages, and the fibroblasts lay down precursors of scar

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Repair Stage• During this phase, collagenous tissue is

synthesized and deposited by the fibroblasts

• Certain nutrients are required for this formation - Vitamin C, manganese, magnesium, zinc, copper, iron, methionin, and cysteine

Future Inflammation

• Immature collagen, as it matures, undergoes contraction

• This explains why immobilization for extended periods after injury yields restricted motion of body parts, joints, etc.

• This contraction occurs from 3rd through the 14th week, but may continue for up to 6 months

• Usually, matrix metalloproteinases allow for homeostatic deposition and degradation, but during this phase, deposition is 40X degradation

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• During this phase, H bonds are replaced by covalent bonds, and later cross links form between adjacent collagen filaments

• At 3 weeks post injury, this tissue is only 15% of normal max strength

• Thus, light handling, without maximum resistance, is indicated

• Excessive handling may further damage, and inflame the area, with additional scar formation

Remodeling Phase

• This is the scar reorganization phase• This may extend more than 1 year, and

the resultant tissue is typically weaker than original tissue

• This weakness may contribute to hypermobility, DJD, and IVD weakness and predisposition to injury

• Low load, long duration stress may help to achieve elongation of this connective tissue

• (ie traction beginning 2-3 days post trauma)• Muscle tension, movment, fascial plane glide,

and mobilization of soft tissues, as well as its loading and unloading, effect scar tissue formation

• Thus STM and traction should be employed to allow for recovery of the condition, and to achieve best possible recovery

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Stage 1

• Lasts 0-72 hours• Tx should be focused on inflammation

reduction for previously mentioned reasons

Stage II

• May be delayed, or prolonged, and is often prolonged due to repetitive injury

• Vigourous activities of daily living, management, exercise, etc. may delay this

• Treatment is focused on allowing scar formation to establish strong connections, but align fibers for maximum strength, reduce pain, return joint function, etc.

Stage III

• Most variable in duration• Management resolves around

contraction and management of scar tissue formation

• Return of ROM, prevention of limitations, management and prevention of DJD, etc.

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The type of vehicle Matters

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Concepts of Whiplash Injury Development

• The cause of pain related to whiplash has classically been attributed to the stretch and tearing of the contractile elements. This is consistent with long term complaints and the delay of the onset of symptoms, however, some other factors seem to call this theory into question

Recent Study• Long term studies on enzymes do not support

the concept of continued primary muscular damage in cases of persistent whiplash (EurSpine Journal (2002) 11:389-392

• Creatine kinase was measured in serum in patients following whiplash injury

• The findings failed to demonstrate elevated levels in most at time of injury (in all but 2 of 25 subjects.

• All levels returned to normal within 48 hours post injury

• No elevated levels were seen in any patients following that time frame, whether chronic symptoms were present or not.

• This seems to indicate that large amounts of muscular damage are not a primary perceptible cause of the symptomatology of whiplash injury

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• First, the majority of neck pain following CAD is not of the anterior muscular groups. These groups would be the first stretched and thus torn with rear impact MVAs.

• Also, these groups are smaller and also are further from the axis of rotation of the cervical spine, so one would expect more significant injuries to occur to these groups.

• The head will fall anterior (the axis of rotation) is anterior to the foramen magnum, so the posterior musculature is required to maintain the head in an erect posture within a gravitational field, and thus are larger and stronger

• Also, long term persistent symptoms following MVA are typically not localized to the anterior cervical spinal musculature, but are of the posterior cervical spinal regions

• One of the current thoughts is that the facet joint is the source of the chronic pain in the majority of patients that suffer persistent pain following CAD.

• This is thought to be due to referred pain patterns, with the muscle being the referent organ for the pain.

• This may also be due to local motor control and feedback cycles at a cord level.

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• It has also been noted that experiments have produced tears in the ALL and rim lesions, which were not evident on radiographs

• Also, research on pigs have shown changes in the spinal canal pressures that occur as the neck moves through flexion and extension

• These tests were comparable with moderate form of CAD trauma in humans.

• These animals showed no obvious neurological signs, but did have mimimalcapsular bleeding in the cervical ganglia were found

• It was later determined that the C4-7 spinal ganglia had lost their normal blood-nerve barrier

• It is believed that this might explain some pain that develops following CAD

• Some researchers believe that these findings, along with findings of RBCs and and increased protein in CSF are significant

• It is believed that due to the spinal canal volume decreasing with extension, that the spinal cord surrounded by fluid, is damaged with rapid extension of the c spine

• This fluid cannot be compressed, and the spinal cord thus would suffer injury with rear impact MVAs

• This is true even with the initial sheer effect seen in CAD trauma

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Seat Position• The position of the operators seat is

important as to where the vectors of force may fall on a patient

• Most individuals recline their seats 20-30 degrees

• With seats inclined at 20 degrees, capsular strains occurred at C2/3 and C3/4 (with more strain at the latter)

• With seats inclined at 0 degrees, the capsular strain occurred mainly at C5/6

Unusual Mechanisms

More Facts

• Rear impact MVA’s are the vector of force that produces cervical spinal injury most frequently.

• This is a biphasic injury, with a component of extension and flexion.

• The frontal impact is monophasic with only a flexion component.

• Although the posterior muscles are of greater clinical significance.

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Rear Impact• In Pain Res. Management Journal 2003,

kinematics of low speed rear end impacts were evaluated.

• These were determined to have the following effects:

• While the whole cervical spine was in extension, the upper cervical spine segments were in relative flexion while lower cervical spine segments were in extension

• Facet joint capsular stretch was seen to range from 17 to 97%, and thus it is believed that injury to these tissues may be a large contributor to complaints.

• The head and T1 were found to accelerate vertically almost instantly after impact, however, movement of the head in a horizontal direction was delayed.

• This elevation of the torso was magnified if the seat back was declined at 20 degrees

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• Posterior shear deformation was also found

• The capsular stretch that occurred secondary to the mild S-shaped curve that occurred during this impact is thought to likely be a source of pain as opposed to muscular injury sources

• Occupants wearing only lap belts have increased incidence of lumbar injury

• If they are slouched, or the torso is flexed prior to rear impact, the affects on the pelvis are worse, as the initial acceleration is that of the pelvis, and forced flexion will occur until the thorax strikes the seat back

• The deceleration that occurs causes the entire upper torso to be restrained only by the lap belt

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• Interesting to note is the fact that cervical spinal injuries are 3X more likely to occur in occupants wearing seat belts

Effects on the Cervical Spine with Rear Impact MVAs

• Authors describe a series of events that occur following impact

• These occur in the following order:– compression, tension, shear force, flexion

and extension– These occur at different levels in the neck

• Compression occurs immediately after impact as the thoracic kyphosis straightens (as the seat pushes on the thoracic spine)

• Then, the weight of the torso and seat belt pull down the torso and tension thus rapidly occurs in the neck (the head lag phase)

• This causes a shearing force that is transmitted from one vertebrae another

• This allows for straightening of the cervical spine, and generates a flexion moment of the C spine (greatest in upper C spine)

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• The overall effect is flexion of the upper C spine, with extension of the lower C spine

• This results in an “S” shaped curve of the cervical spine following impact

Rear Impact Sequence of Events

• The effect of rear impact injury on the cervical spine have been divided into four phases by some authors

• These phases explain the local effects that occur to the underlying anatomy of the cervical spine

Phase I

• With impact, the vehicle begins to accelerate• Initially, the pelvis and lumbar spine push the

seat backward, and the seat may store some potential energy to return to neutral position

• (It should be noted that the best position for the head rest should be even with the top of head and resting against the headrest)

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• Integral head restraint systems, built into the seat back, are more effective at reducing injury that adjustable head rests

• Other studies have indicated that head rests do not alter the incidence of neck injury

• Again, this may be due to the improper use of the head rest

• Different studies have shown that male drivers have had their head rests too low in 74 to 90% of those investigated

• Even if adjusted properly, elastic recoil and effect of the upper C spine being forced into flexion at the time of head strike may create injuries to the C spine

• New concepts in controlled collapsing seat backs are being proposed to reduce injury, but the ability to control the vehicle post impact is an issue

• Due to this unobtainable position typically, headrest do little to effectively reduce C spine injury

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• As the seat back pushes into the occupant, the thoracic kyphosis is decreased - this causes– increases vertical torso height– induces vertical acceleration of the

head/neck– compresses the entire spine

• Sequential sheer stress moves up the cervical spine from segment to segment

• The further the occupant sits away from the seat (backset) the greater this sheer stress

• This is occurs with the S shaped C spine curve which has flexion of upper C spine and extension of the lower C spine

• This tends to increase facet imbrication in the lower C spine, and possible capsular strain forces

Rotation at the time of Impact

• It has been noted that with rotation at the time of impact, the maximum capsular strain occurs in the contralateral capsules in reference to the side of rotation versus neutral positioning

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• As the torso pushes into the seat, the head and neck undergo tension, as they are accelerating in the posterior direction

• This imparts sheer stress to the C spine, and the greater the backset, the greater the potential for injury

• Significant injury may occur prior to the head ever striking the headrest

• Phase II now begins with this head lag

• Some interesting facts are that males tend to load the seat backs more due to greater mass, so that they accelerated less rapidly

• Males have a greater extension phase• Thus males tend to be injured more in the

initial phases of impact• Females tend to be injured in later phases, as

they accelerate more rapidly, and are pushed off of the seat back more violently

Phase II

• Coincides with head strike• It is known that if the headrest is too low, the

neck will increase it’s extension, and the headrest will act as a fulcrum to increase the injury effect on the cervical spine

• High head restraints are best• Often, if the seat back does not break, in this

phase it will begin to rebound, adding to the occupants forward acceleration phase

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Not So Mild Trauma!

Phase III

• Begins as the occupant begins to move forward

• This motion can be accentuated via the shoulder restraint mechanism

Phase IV

• This forward movement is often stopped by the shoulder restraint, and this increases the stress on the neck

• Accentuation of the flexion of the lower C spine occurs due to this

• The time for stretch response of muscle (120-170 msec) is not sufficient for prevention of injury with extension, but may contribute to flexion in phase III

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TMJ Injuries

• Injuries or disorders of the TMJ, are often undiagnosed, misdiagnosed, or ignored

• This is due to poor understanding, as well as the common nature of dysfunction of this articulation

• A large percentage of the population reports symptoms that are associated with TMJ dysfunction (88%)

TMJ Proprioception

Neurologic Connections

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• Thus it is difficult sometimes to fully apply a causitive agent to a dysfunctional joint

• These injuries are often manifest clinically due to MVA, however, preexisting subclinicalfindings of dysfunction are often present, thus predisposing the patient to injury and symptomatic dysfunction following injury

• When injury to the TMJ is present, evaluation of dentition is essential to eliminate or identify this as a causitive or possible resultant area of dysfunction

• Altered occlusion may cause proprioceptivechanges in the TMJ, which are viewed as “normal”

• This abberent view of vertical and horizontal orientation and function may lead to alterations in muslce tone and function, and joint movements

• The effect on the bony and contractile elements may lead to injury, or inappropriate resolution of inflammatory processes

Review of TMJ Anatomy

• This is a synovial articulation with an intra-articular disk, which truly is a two compartment joint

• The joint is comprised of the mandibularfossa of the temporal bone, as well as the condylar process of the mandible

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• Of interest, is the mechanics of the joint• The fiborcartilagenous disk divides the

cavity of the TMJ into two compartments (upper and lower)

• The mandiblue head move forward with opening, and the disk moves with this

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• Anterior to the mandibular fossa is the anterior tubercle

• This prevents anterior dislocation of the mandible, and its orientation is critical in jaw function

• The convexity of this struction is variable, and may predispose anterior disc slippage or dislocations (jaw opening versus closing locks)

• The articular disk is biconcave, with no innervation or vascular supply

• It is thicker medially, and the thinner lateral portion is more predisposed to tears

• The disc self centers in the fossa, and continually changes conformation with joint movement

• It moves with the condylar head as a functional complex

• Behind the disc is the bilaminar zone containing the retrodiscal tissue

• This tissue is clinically important is it is very vascular, and innervated

• Injury to this thus will produce pain, inflammation, and possible maloccclusion

• Hemarthrosis may occur with fibrotic changes occuring, restricting joint motion, and potential limitation of disc motion

• This often produces the common audible “pop” noticed by patients

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Ligaments

• Discal collateral - attach to medial and lateral portion of disc and help to divide the joint as mentioned

• Capsular ligament - surround the joint, and resists inferior and medial and lateral displacement

• The lateral aspect of the capsule is thickened to form the tempormandibular lig

• The temporomandibular ligament has both an inner horizontal band and an outer oblique band

• The outer oblique band aids in transition from rotation to anterior glide and translation

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Muscles of Mastication

• Masseter - is superficial overlying the lateral aspect of the ramus of the mandible– takes origin from the zygomatic arch and

zygomatic bone– inserts onto the inferior lateral aspect of

ramus and angle of mandible– its action is to elevate the mandible– innervation is via the anterior division of V3

• Temporalis muscle– superior and deep to masseter, this muscle

takes origin from the temporal fascia and temporal fossa

– it inserts onto the anterior portion of the coronoid process of the mandible

– main action is elevation of the mandible– also innervated by the anterior division of

V3

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• Medial and lateral pterygoid muscles– medial takes origin form the pterygoid

fossa and tuberosity of the maxilla– inserts on the medial surface of the ramus

and angle of mandible– main action is elevation of mandible

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• Lateral pterygoid– takes origin from the infratemporal surface of

sphenoid bone and lateral pterygoid plate– insertion is onto temporomandibular joint capsule

and condylar process of mandible– This muscle has both superior and inferior

divisions, the superior connects more with the capsule of joint and elevates mandible

– the inferior division aids in depression or opening of mandible

– These also provide for medial translation of the mandible

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Mechanics

• The TMJ initially upon opening moves in a rotary fashion around a coronal axis

• This rotation is accomplished in the first 12-15 mm of movement, followed by anterior movement of the condylar head for the next 60 mm

• This subsequent gliding motion results in anterior displacement of the condylar head

• Typical mechanism of “jaw lash”• Predisposing factors• Direct trauma• Injuries during treatment with traction,

etc.

Crash Vectors

• Must be considered as their influence directly contributes to the injuries suffered

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Front Impact without Airbag

With Airbag

Frontal Crashes

• Occupants can often brace for impact• This is the most common vector of

crash, but does not create the greatest proportion of injury, rear impact does

• Responsible for 1/3 of acute and long term cervical spinal injuries

• More neck injuries are seen in drivers that forcefully clench the steering wheel

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• Front impacts create the most severe injuries• Additional protection is afforded to the driver

by the engine, steering wheels, floorboards, etc.

• Although they afford protection these internal components are also responsible for many additional injuries that would not be seen with rear impact injuries

• “Dive down” of the striking vehicle occurs with this type of impact

• This will help to alleviate direct forces supplied to the front of the vehicle, but may cause other injuries depending on the amount of dive down that occurs

• Observe the “Dive down” that occurs in the following video

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Frontal Impact

• Risk for injury -– at 0 - 5 mph about 8 %– 11 - 15 mph about 30 %– 15 - 20 mph about 35 %– 20 - 25 mph about 25 %

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Frontal Impact (Primary Deceleration) and Tissue

Injury• Tissue injury, as expected is focused on

elements that are in the posterior distribution of the cervical spine, at least initially

• Facial trauma is a consideration, as is fractues of skull, anterior vertebral body, avulsion fractures, etc.

Side Impact Crashes

• Risk for injury is about the same as for frontal crashes

• Intrusion into the vehicle and head strike against interior of car are concerns

• Low back injuries often present due to no lateral support of the thorax

Impact Without Protection

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Side Impact with Airbag

Note also resistance to lateral Movement

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• With these vectors of injury, no or little protection is afforded to the occupant for lateral sheer forces or lateral acceleration

• A increased level of lumbar spinal injury is seen in these patients

• This mechanism of injury causes the immediate acceleration of the occupant toward the striking vehicle

• The articular structures on the ipsilateral side of impact undergo compression

• The soft tissue structures, both contractile and non contractile on the side opposite of impact undergo lengthening

• This contributes to soft tissue injuries, as the response of these tissues to stretch that is not autogenerated is that of contracture

• Given this, a lap belt supplies an anchoring apparatus to act as a fulcrum for lateral flexion, increasing lower back injuries

• Interestingly, lower back injuries are more common with only lap belts worn in rear end impacts

Side Impact Tissue Injuries

• Contractile versus non contractile injuries

• Traction plexopathies

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Occupant Position

• Effects risk of injury• With rear impact - rear seat passengers

have less C spine injuries• Front seat passengers have a greater

risk of injury than drivers or rear seat passengers (with rear impact)

Rear Seat Passenger with Frontal Impact

Rear Seat Passenger Effects

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Differences in Injury Risk• The taller the occupant, the greater risk of

neck injury• Females tend to have a 2X risk of injuries to

versus males• Occupants over 30 years of age have a

increased risk of injury• Young children have a decreased risk of

injury• Bracing for impact reduces injuries

• Additionally, rapid deceleration in the latter phases of a rear end impact magnify the effects of the injury

• Rapid deceleration occurs with striking another vehicle, or with the three point restraint system currently used

• July 2003 study in Med Clin. Journal revealed a worse prognosis in the following patients following MVAs– whiplash affects young people equally based on

sex in rear end collisions– Worse prognosis was seen with increased age,

female sex, increases in severity of the initial clinical symptoms, previous cervical pathology, and abnormal cervical MRI or CT

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Recent Study• Journal of Biomechanics September 2003,

revealed that segmental angles were greater in females at the C2-3, C4-5, C5-6, and C6-7 areas.

• This was during the loading phase of rear end mechanisms of injury

• This intersegmental increase in motion, and it’s effect on local tissue, may explain the increased injuries and complaints seen in females following MVAs

Recent Study

• Pain Res. Management Summer 2003, determined a number of factors that were related to prolonged recovery times from whiplash injuries. These included:– older age– female gender– having dependents and not being

employed full time

• It was found that each of these decreased recovery time by 14 to 16%

• Factors related to crash conditions that prolonged healing times were:– being in a truck or bus decreased recovery by

52%– being a passenger in the vehicle decreased

recovery by 15%– colliding with a moving vehicle decreased

recovery by 16%– side or frontal impact decreased recovery by 15%

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• This study also indicated signs and symptoms that increased recovery time. Beside female gender and older age, these included:– neck pain on palpation– muscle pain– pain or numbness radiating from neck to

arms, hands or shoulders– headache

• This study utilized 4,759 patients• In a group of patients with signs and

symptoms, the median recovery time was 32 days, however, 12% had not recovered after 6 months

• The presence of all the factors listed (headache, muscle pain, etc.) in females aged 60 predicted a median recovery time of 262 days, compared with 17 days for younger males 20 years old that did not have any of those symptoms

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Experimental Tissue Injuries

• With frontal impact, the following structures tend to be damaged with increasing forces in animal models:– transections of cord, vertebral artery

thrombosis, – atlantoocciptial separation, basil skull

fracture– posterior musculature, tectorial membrane

and PLL

• With rear impact experiments, the following tissues have shown injuries– transections of the cord– esophageal hemorrhages, aortic

hemorrhages,– brain injuries– muscular injuries, ligamentous injuries of

ALL, cord contusions

Recent Study • Spine 2003, it was found that following

whiplash, patients demonstrated an increase in trunk lateral sway, roll, and velocity versus control individuals.

• This increase in trunk sway is noted to occur during complex gait tasks that required task-specific gaze control - ie stairs

• Trunk sway was less with activities that involved simple tasks with gross head movements, without task-specific gaze control

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• Thus, it appears that patients with chronic whiplash demonstrate increases in trunk sway different than other patients with balance problems

• This may be due to alterations or a pathologic vestibulo-cervical interaction.

• This may lend credibility to enhancing proprioceptive alertness via plasticity following stimulation of joint afferents as well as spindle receptors.

• Thus, trauma may be a cause of long term degerative joint disease, but other factors must be considered as well

• Studies show a 6x increase in degenerative changes in CAD patients versus contols

• If these patients suffered a LOC, they had a 10x fold increase in degenerative changes

Recent Study• A recent study (Neuroradiology 2003)

demonstrated damage to the tectorial and posterior atlanto-occipital membranes and did so via high resolution MRI.

• This study was done on individuals several years following the CAD injury, and are classified as permanent

• These injuries elongated or ruptured the atlanto-occipital membrane-dura complex and thinned the post atlanto-occipital membrane and tectorial membrane

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Recent Study Information

• According to Pain Journal, May 2003 the following information is submitted.

• Dysfunction in the motor system is a feature of persistent whiplash associated disorders

• Parameters of ROM, joint position error, as well as activity of neck flexors were utilized

• All whiplash subjects demonstrated decreased ROM and increased EMG at 1 month post injury

• Interestingly, this persisted in the moderate and severe symptom group, but returned to normal in mild symptom group at 3 months

• Increased EMG persisted in all groups at 3 months

• So, motor system deficits are found at 1 month post injury, and were persistant in all groups at 3 months, whether the symptoms were present or not

Recent Study• Long term studies on enzymes do not support

the concept of continued primary muscular damage in cases of persistent whiplash seminars (Eur Spine Journal (2002) 11:389-392

• Creatine kinase was measured in serum in patients following whiplash injury

• The findings failed to demonstrate elevated levels in most at time of injury (in all but 2 of 25 subjects.

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• All levels returned to normal within 48 hours post injury

• No elevated levels were seen in any patients following that time frame, whether chronic symptoms were present or not.

• This seems to indicate that large amojunts of muscular damage are not a primary perceptible cause of the symptomatology of whiplash injury

Injuries of the Nervous System following MVA

• Whiplash may produce neurologic damage• This injury may encompass the central or

peripheral nervous systems, and thus the clinical signs and symptoms are significantly different

• Some of these injuries may be permanent, and thus may necessitate appropriate evaluation

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• CNS injuries can occur to the brain, brainstem, or spinal cord

• Brain injuries can occur due to cranial fracture, in which the brain may be directly contused

• The superficial tissues may be lacerated, and if opened, the dura may also be lacerated.

• Additionally, if the cranial vault is opened, the possibility of post traumatic infection should be considered

• Cranial injury may also produce hematomas -these may be epidural or subdural

• Epidural hematomas are usually arterial, rapidly developing, and may involve the middle meningeal artery

• These may produce brain displacement, lucid intervals, as well as herniation syndromes

• These are extremely serious, and must be recognized immediately, and appropriate txbegan immediately

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• Subdural hematomas are usually venous in nature, and elderly individuals are predisposed to this due to the sheering effects of vein in the subdural space

• These tend to be of a more sublte, delayed develoment, and may become chronically present in the patient

• These may also produce local tumor-like signs, or may produce herniation syndromes, depending on their location and speed of develoment

• Signs and symptoms of epidural and subduralhematomas include:– lethargy– decreased level of consciousness– pupillary diameter changes– nausea– vomiting– veritgo– sensory changes– motor changes– HA, diplopia, LOC, etc.

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Brainstem Injuries

• Brainstem injuries may occur due to the excessive force, torque, or stretch placed on this portion of the NS.

• However, due the location of vital centers in the brainstem, such as respiratory and cardiac regions of the medulla, traumatic lacerations/injuries here are often fatal, and chiropractic care is not beneficial

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• Brainstem injuries may be identified by a number of clinical keys:– evaluation of cranial nerve function– assessment of function of long tracts that

course through the brainstem along with the cranial nerves

• Horizontal gaze palsies have been identified due to damage of the abducens nerve or potentially the paramedian pontine reticular formation (PPRF)

• Hematoma formation must also be considered

• Vascular infarctions may occur secondary to traumatic injuries that initial immediate or delayed Wallenberg syndromes via arterial spasm, thrombus, or emboli

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Spinal Cord Injuries

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• Spinal cord injuries can occur, and young children are at a greater risk for these

• This is due to decreased muscular mass, strength, and development

• Increased risk of cord damage are also seen in cases of ligamentum flava buckling, ossification of the PLL, herniations of nucleus pulposus, etc.

• Root Syndromes may occur in which damage to a particular nerve root occurs, potentially giving rise to dermatomal sensory changes, or myotomal motor changes, reflex changes, etc.

• Central cord syndrome may occur, especially with significant cord trauma

• This may be accompanied by vertebral fracture, and central portions of the cord tend to be altered in their function

• Thus, a central cord syndrome would typically initially include alterations in perception of pain/temperature, and commonly occur secondary to syringomyelia formation in the cervical spinal cord

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• Anterior cord syndromes may also be generated secondary to MVA

• This affects the distribution of the anterior spinal artery, and results in preservation of accurate touch modalities for the most part, with damage to and loss of pain/temp as well as volitional paralysis distal to the lesion site

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• Complete transection of the cord may occur

• Obviously, there is a loss of all volitional motor activity and sensation distal to the injury site

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• Although these appear as distinct clinical entities, it appears that they may be one entity, that is altered in the clinical picture secondary to vector and amount of force

• Injuries of lower magnitude to the cord seem to affect only the anterior and posterior horns

• Thus, root syndromes develop• These may be unilateral or bilateral • The distribution depends on the position

of the head during impact as well as direction of force application

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• The central cord syndrome has the same cause, but the vectors of force damage different structures

• Thus the damage spreads to central part of cord, and possibly anterior horn cells for the upper extremity

• Thus pain fibers as well as fibers for bladder control in the anteriomedial gray matter

• Anterior cord syndrome evolves as forces increase, and are transmitted to more of the gray matter, and anterior and lateral funiculi

• The dorsal funiculus remained spared• This is consistent with the distribution of the

anterior spinal artery• The gray matter is these cases is known to

undergo long atanding changes not seen in the white matter of the cord

• Oblique vectors of force alter the distribution of forces on the cord

• These cause the summation of forces to be applied to the posterior and lateral funiculus, and in effect give rise to a Brown-SequardSyndrome

• This has a classic presentation of ipsilateralaccurate touch, contralateral pain and temp, and ipsilateral voluntary motor functional losses

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Diffuse Axonal Injury

• Most common cause of vegetative state and severe disability following injury

• aka diffuse degeneration of white matter, shearing injury, diffuse damage of immediate impact type, diffuse white matter shearing injury, inner cerebral trauma

• Now DAI is the term

Post traumatic Headache - the Post Concussive Syndrome

• Headache is the 2nd most common complaint following MVA

• Headaches that are traumatic in nature may arise from direct cranial trauma, or from injury to the underlying neurlogic tissue from the brain

• Additionally, damage or changes in chemistry of injuries tissues may contribute

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• Etiology Factors for Posttraumatic Headaches– Head contact - 57.3%– Whiplash 43.6%– Object (free object) hit head - 13.7%– Body was shaken - 9.4 %– Other 13.7%

• Recent studies have demonstrated a sensitization of the underlying trigeminal system that occurs following trauma

• This sensitization causes stimuli that may ordinarily be interpreted as normal to be inappropriately determined as being painful

• Also, this system may give rise to spontaneously generated action potentials that when present in a nociceptive system are interpreted as painful stimuli

• However, even if damage to all the aforementioned tissues can generate headache conditions, due to the currently available studies it seems viable that other causes must be considered

• This is due to the finding of DAI (diffuse axonal injury) in MTBI (mild traumatic brain injury)

• This injury to axonal tissue of the CNS has been thought of as psychogenic in the past, however is well documented

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• This injury has a range from small regions of axonal shear, to large regions of evident axonal injury

• Most often, the injury to these axons in non detectable on radiographs, CT, MRI, EEG, CSF evaluation, etc. (PET scans have shown promise in their diagnosis but are not currently the assessment tool of choice clinically)

Diffuse Axonal Injury

• Most common cause of vegitative state and severe disability following injury

• aka diffuse degeneration of white matter, shearing injury, diffuse damage of immediate impact type, diffuse white matter shearing injury, inner cerebral trauma

• Now DAI is the term

Examples of DAI

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• Three distinct findings in DAI– focal lesion in corpus callosum often involving the

septum and associated with intraventricularhemorrhage

– focal lesion in one or both dorsolateral quandrantsof rostral brainstem

– microscopic evidence of damage to axons

– First two may be identified – Third can only be identified histologically

• Multiple axon bulbs can be identified in acute injuries

• MC in parasagittal white matter, corpus callosum, IC, thalami and in ascending and descending tracts of stem

• Later, large numbers of small clusters of microglia can be seen throughout white matter of hemispheres and in brainstem

• Bulbs most effectively seen within 2 weeks of injury

• Clinical course - these patients have lower incidence of lucid interval, fx, contusions, hematomas, and evidence of increased ICP, as compared with with patients without this injury

• Usually associated c MVA• Known to exist in varying degrees of severity,

and in a continuum from concussion up to persistent post-traumatic coma

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• Grades of DAI• grade I - histologic evidence only throughout

white matter, no focal accentuation in CC or stem

• grade 2 - widely distributed axonal injury, and focal lesion in CC

• Grade 3 - most severe, and end spectrum of disorder, has diffuse damage to axons in presence of focal lesions in both CC and in stem

• It appears the mechanism is initial damage to axon at nodes of Ranvier where there is fragmentation of axolemma - called primary axotomy

• This is due to axonal shearing and resealing of fragmented axon within 60 minutes post injury

• With survival there is accumulation of transported axoplasm and organelles, This disrupts the axollema and undergoes secondary axotomy

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• Secondary axotomy is believed secondary to calcium influx that activates proteases that degrade membrane proteins and neurofilaments

• Another theory states that dirsuption of axonal transport results in mictotubularand neurofilamentous disturbances of cytoskeleton

Symptoms of PCS (DAI)• Lightheadedness, Vertigo, dizziness, neck

pain, headache, photophobia, phonophobia, tinnitus, impaired memory, easy distractibility, impaired comprehension, forgetfulness, impaired logical thought, difficulty with new or abstract concepts, insomnia, irritability, apathy, anger, mood swings, depression, loss of libido, pesonality changes, and intolerance to alcohol

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CASE TIME!!!

Relevant Signs and Symptoms• 22 year old woman suddenly developed

posterior neck pain, vertigo, ataxia, left facial numbness, and hoarseness after cervical HVLA.

• 4 months prior to presentation, patient injured her neck in an MVA. Following HVLA by a DC, the patient suddenly felt increased pain in the left posterior neck region. She then noticed increased dizziness and nausea an staggered out to her car from the office of the DC.

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Relevant Signs and Symptoms• She was noted to be falling toward the left

during her staggering episodes. She noticed her vision bouncing or swaying, but denies diplopia. She vomited twice, and when she returned home, her husband noted that her voice sounded hoarse. She experienced numbness and tingling on the left side of her face. She decided to take a nap, and when her symptoms did not improve, she presented to the ER.

Examination Findings• T 96, pulse 60, BP 126/84. Neck, supple with

no bruits, lungs CTA X2, Cardiac exam RRR, abdomen soft nontender, and with normal extremities.

• Neurologic exam - AOX3, normal language, named months forward and backward with no errors. Recalled 3/3 words after 4 minutes. Left pupil 2.5 mm, constricting to 2mm, right pupil 3.5 mm, constricting to 2 mm, visual fields full. Right beating horizontal and counterclockwise rotatory nystagmus, increased with rightward gaze. Patient reports an associated perception of visual field moving back and forth.

Examination Findings

• Extraocular movements full, left ptosis, decreased pinprick and temperature sensation in the left V1 V2, and V3 divisions of V, decreased left corneal reflex, face symmetrical taste not tested. Hearing intact, voice hoarse. Decreased palate elevation on the left, and decreased left gag reflex. Normal SCM and trapezius strength. Tongue protruded in midline.

• Motor - no drift, normal tone, and 5/5 power throughout

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Examination Findings

• Reflexes - all DTRs bilaterall and symmetric, no Babinski or Hoffman’s signs present.

• Coordination - Mild ataxia on finger to nose testing on the left, toe tapping on the left was irregular in rhythm. Patient unable to stand due to dizziness, decreased pinprick and temperature sensation in the right limbs and trunk below the neck. Intact light touch, vibration and joint position sense.

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KEY SYMPTOMS AND SIGNS• Pain in the left posterior neck region

• Unsteady gait, falling toward the left

• Left ataxia and dysrhythmia

• Dizziness and nausea with right-beating nystagmus

• Decreased pinprick and temperature sensation in the left face

• Decreased left corneal reflex

• Decreased pinprick and temperature sensation in the right limbs and trunk below the neck

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KEY SYMPTOMS AND SIGNS • Left ptosis, with small, reactive left pupil

• Hoarseness, with decreased palate elevation on the left and decreased left gag reflex

Sensory Testing

RELEVANT ANATOMICAL & CLINICAL CONCEPTS• Anterolateral Pathways

• Trigeminal Sensory System Nuclei and Pathways (CN V)

• Sympathetic Pathways Causing Pupillary Dilation

• Vestibular Pathways (CN VIII); Vagus Nerve (CN X)

• Localization of Ataxia

• Brainstem Blood Supply

• Ischemic stroke mechanisms, diagnosis, and treatment

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Left Laterally Medullary Infarct at Patient Admission Time

Left Laterally Medullary Infarct, at Five Day Follow-up

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Left Laterally Medullary Infarct at Patient Admission Time

Left Laterally Medullary Infarct at Patient Admission Time

FINAL DIAGNOSISLeft vertebral dissection causing left lateral medullarysyndrome (Wallenberg’s syndrome)

OUTCOMETreated with anticoagulation to reduce risk of recurrent stroke. Marked improvement of all abnormalities at 11-day follow-up, with only mild residual deficits.

Numbness, Hoarseness, Horner’s Syndrome, and Ataxia

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Intake form

• Patient Information

• Name, date, personal info

• Accident Information

•When, where, who, how direction, conditions, etc.

Intake Form (cont.)

• Consultation

• Chief Complaint

• Onset and Course / OPPQRST

• Childhood Hx

• Adult Hx

• Operations

• Injuries

Intake Form (cont.)

• History of past illness

• Family history

• Social History

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Intake Form (cont.)

• Systematic Review

• General

• Skin

• Head – EENT

• Neck

• Respiratory

• Cardiovascular

Intake Form (cont.)

• Systematic Review (cont.)

• Gastrointestinal

• Genitourinary

• Gynecological

• Locomotor

• Neuropsychiatric

Intake Form (cont.)• Exam

• General

• Vitals

• Systems

• Georges Test

• Neurological Test

• Orthopedic Test

• ROM

• Palpation

•Films

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Daily Visit

• Verification of Services

• Self Release

• Termination

• Advice

• Narrative

Course End

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• Peripheral nervous system injury occurs secondary to IVF encroachment, stretch, or other compressive events

• Mild compression can occlude the epineurialveins, raising intrafunicular pressure, potentially generating axonal damage

• Stretch of the nerve by 8% produced venous stasis, whereas 15% stretch generated complete ischemia of the nerve

• Traction injuries occur most commonly with forced lateral flexion of the c spine

• Lateral mechanisms of injury, or forced lateral flexion - ie shoulder point and head falls from motorcycles, etc.

• The initial phases of pns injuries are always painless, and thus may not be reported by patient

• The long term resolution factor is most dependent on endoneurial maintenance

• Classes of injuries are as follows:• Stage 1 - axon injury/endoneurial spared• Stage 2 - axon injury/Wallerian effects • Stage 3 - axon and endoneurium disrupted• Stage 4 - axon and perineurium disrupted• Stage 5 - complete transection of nerve

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Compressive Mechanism of Injury (Also seen with

Traction)• Mechanical deformation of the nerve

can be responsible for nerve lesion, but ischemia also is present

• The effects of compression are dependent on multiple factors. These factors include the following:

– Rate of deforming force application – Local or diffuse are of compression– Amount of force – Regional anatomical susceptible zones– Internal structure of nerve at compression

site– Health of patient

Acute Nerve Compression

• Mildest form of lesion, conduction is lost, and this loss of conduction is believed secondary to ischemia

• Full recovery occurs• Pre and post ischemia findings occur -

these include pain, parasthesias, and hypersensitivity

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Chronic Compressive Lesions

• The initial vascular disturbances introduced by compression are that of venous ballotment and congestion

• This also results in capillary stasis• Nerve fibers and capillary endothelium

are very sensitive to this stasis

• In order to maintain an adequate intrafunicular circulation for the nutrition of nerve fibers the pressure in the system much be such that – pressure in arteries in epineurium must be greater

that that in the funicular capillaries, which must be greater than the intrafunicular pressure, which must be greater than the epineurium containing veins that drain the tissue, and their pressure must be greater than the pressure in the tunnel that the nerve is located within

– Pa>Pc>Pf>Pv>Pt

• When tunnel pressure increases, the epineurial veins suffer first

• This leads to hyperemia, venous congestion, and slowing of circulation all tissues

• This increases the local pressures which ultimately lead to pathological changes, the worst of which occurs within the funiculus

• These damages occur in stages

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Changes that occur at the site of Neuronal Injury

• These changes seem to be dependent on whether the endoneurial sheath and Schwann cell basement membrane are preserved or not

When the sheath is Preserved

• The effects of neuronal injury are minimal, and usually due to the degeneration of the axon as opposed to the injury itself

• The permeability of the perineurium is increased with the injury

• Mild hyperemia follows this change • Endoneurial edema follows in 1 to 2 hours,

with increased capillary permeability

• Within hours, degenerative changes are noted on each side of the compression site

• By the 3rd day following injury, Schwann cells were found in the area of endoneurium that was damaged, and regenerating axon sprouts were present there as well

• The endoneurial tube remains intact and regeneration has great potential to occur

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Local Reaction following Nerve Rupture

• Following injury, the ends of the damaged nerve retract, due to the elastic propertieis of the endoneurium

• Thus, structures known as retraction bulbs are formed

• Local inflammation occurs with capillary injury and hemorrhage and increased capillary permeability

• Thus, exudate forms that accumulates around the ends of the nerve

• Macrophages invade and endoneurialfibroblasts and Schwann cells multiply and migrate to form bridging

• This consists of Schwann cells and connective tissue that forms a framework with capillaries, collagen and macrophages

Retrograde Fiber Reaction

• These changes occur proximal to the site of nerve injury

• Similar to the effects that occur distal to the injury site

• The distance that this occurs is directly proportional to the severity of the injury

• If the injury fails to disrupt the endoneurialtube, this is usually only the adjacent few mm

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• This may be as great as several cm• The internode survives the injury if the

nucleus of the Schwann cell remains viable (the proximal 1/2 of the cell)

• The degeneration may occur for up to 7 days following the injury

• The proximal axons develop swellings just above the injury

• The last surviving internode is also seen to swell

• The axon swellings are known to contain oxidative enzymes, cellular storage granules, for neurtamsmitters, etc

• This is due to accumulation in this area from impaired axoplasmic flow

• These proximal nerve fibers are known to undergo a decrease in diameter

• Also, a decrease in myelin thickness occurs• Conduction velocity proximal to the injury site

is thus slowed, and this often remains even after re-innervation of the end organ

Retrograde Cell Reaction (The Axon Reaction)

• This does not always happen if the axon is injured

• The initial phase has been listed as a reactive phase

• The cell itself may or may not recover from this phase

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Reactive Phase

• Nucleus displaced to periphery• Nucleolus enlargement• Nissl dissolution - fully complete by

about 4 days following injury• Cellular swelling occurs - believed due

to water uptake and increase in organic material

• Lysosomes increase in number• Controversy seems to exist as to the effects

of injury on location of the Golgi apparatus, endoplasmic reticulum and other cytoplasmicorganelles

• The cytoskeleton is known to undergo change and become disarranged

• Again, the cell may or may not survive following these changes

• The glial cells surrounding the neuron also undergo changes

• They proliferate in number, and size with 24 to 48 hours

• This peaks within 1 week with the effect being greatest on the microglial cell

• This process, also effecting the astrocyte, seems to be mediated by chemicals that are released by the injury neuron

• The microglia, if the injury is severe enough, may also act to loosen and displace synaptic connections with the neuron soma

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• This reaction has been considered to improve conditions for recover and establishing new routes of transport between neurons and blood vessels

• This also allows the undisturbed neuron to regenerate a new axon

• If the neuron survives, the glial cell activity is then supressed

• If the neuron dies, the microglia phagocyticrole comes into play

Recovery

• The time before onset of recovery is usually two to three weeks, but varies dependent on the severity of injury

• Recovery seems to continue to the neuron from the 8th to 10th week

Cellular Death

• Neurons that are going to die show the same initial signs

• Degeneration then proceeds at varying rates, again dependent on multiple factors

• The percentage of neurons that die following trauma to the axon vary from 20 to 75%

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• Also noted are increases of polysynaptic discharges, alterations and failures of synaptic transmission, altered integration, etc. have been noted in neurons undergoing this degenerative condition

Factors that influence the Severity of the Axon Reaction

• Severity of injury - direct correlation• The level of injury related to neuron cell body

- the closer the injury to the cell body, the greater the effect on the cell body

• Type and size of neuron - this reaction is more severe in sensory than motor cells, especially for the small spinal ganglia cells

• Restoration of functional recovery with the periphery

• It has additionally been observed that with cellular injury, their may be effects on the postsynaptic neurons in the same pathway

• This finding may cause entire pools of neurons that are postsynaptic to the injured neurons to be in jeopardy of being injured

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Reactions distal to injury Site

• Sometimes referred to WallerianDegeneration

• These signs in the axon are seen 12 to 48 hours following injury

• 48 to 72 hours post injury, the axon breaks into twisted fragments which become dispersed

• All traces of the axon lost by the second week

• Mylein deteriorates and pulls away from the axon

• The entire axon degenerates simultaneously along the length of the fiber, however some authors show evidence of distal degeneration occurring intially

• 36 to 48 hours post injury, myelin degeneration is well underway, and phagocytosis of myelin debri is occurring

• The ability to conduct action potentials is lost, and seems to effect the neuromuscular junction prior to the rest of the nerve fiber

Distal Schwann Cell Activity

• Within 24 hours, the Schwann cells undergo nuclear enlargement, proliferate via increased mitotic activity

• Schwann cell activity declines from about the 2nd to 4th week

• Macrophages are present in great numbers and perform phagocytosis as do some Schwann cells

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• Also noted is the fact Schwann cells and macrophages participate in the clean up of cellular debris

• Mast cells increase in number in connective tissues of nerve when damaged - especially in the endoneurium

• Mast cells also degranulate which liberates histamine and serotonin that increase the permeability of the capillary endothelium which leads to capillary leakage and edema

• Also heparin is released which aids in myelin enzymatic degradation

Specifics about Axonal Regeneration

• The condition of the endoneurial tube is critical

• If intact, the growing axon will tend to regenerate much better

• Regeneration of the axon proceeds smoothly and to completion typically

• After these types of injuries the initial delay is short, and the re-innervation typically to the same end organ and the same pattern

• Function is usually fully restored• However, if the nerve fiber is disrupted,

complications occur• Scar tissue may prevent the axon from

regrowing in the endoneurial tube• So, either regrowth of the axon is delay

due to scar tissue, or may be prevented altogether

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Recovery of the Neuron Cell Body

• Reversal of negative effects occur• Time required for this is directly related

to the severity of the injury sustained• This directly relates to the rate of axonal

regrowth (the health of the soma)• If the endoneurium is intact, growth

buds have been noted 4 to 10 days following injury

• However, this regrowth rate may be delayed for months if the injury to the cell body is severe enough

• This delay of axonal regrowth may be as much as 136 days

• So, the regrowth rate of the axon bud is dependent on– Cell body health– Growth cone itself– The tissue that the axon must grow

through

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• It appears that following regeneration, the speed of transmission remains diminished, although recovery of speed has been seen to be occurring as long as 17 years post injury

• This is believed to be due mainly to thinning of the myelin and increased space of the internodal segments

• Also noted is a 3-4 fold increase in the refractory period of healing nerve fibers

• When an axon is asked to grow through scar tissue formation due to endoneurialdisruption, it undergoes a process of axonal sprouting at the growth bud

• This may give rise to as many as 50 grow buds

• This may result in the formation of neuromas, inappropriate distal re-innervation, decreased numbers of axons available for re-innervation, or alteration in non-myelinated fibers growing into endoneurial tubes of myelinated fibers

Rate of Regeneration

• This varies from organism to organism as well as from nerve to nerve and from the specific conditions of the injury

• This regrowth can be assessed in multiple ways (biopsy, etc)

• Hoffman-Tinel sign may be probably the best for evaluating the regrowth of axons clinically

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Regeneration Rates

• With averages, it appears that the following occurs in reference to regeneration rates (following bridging activity)– Motor 2.77 mm/day– Sensory 3.35 mm/day– (this rate is altered by many things,

including heat - increases rates above 17 C, etc)

Classifications of Severity of Nerve Injury

• Often listed in 5 separate grades• Grade 1 Loss of conduction in axons • Grade 2 Loss of continuity of axons

without breaching the endoneurial tube• Grade 3 Loss of continuity of the nerve

fibers• Grade 4 Loss of perinurium and funiculi• Grade 5 Loss of nerve trunk continuity

Grade 1

• Loss of motor function with sensory loss from the joint, but is always painless

• May be gradual or sudden in onset• Usually no atrophy is noted due to rapid

recovery of axonal growth• Fiber size may explain the first finding,

although it is also noted that sensory findings are more resistant to ischemia for unknown reasons

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Second Degree Injury

• The axon is disrupted• Wallerian Degeneration occurs• Complete loss of sensory, motor and

sympathetic activity• Re-innervation of muscles proceeds in an

orderly fashion according to their original supply, which is opposed to first degree injury in which this is not organized in recovery

• All functions are eventually restored• This type takes longer to recover then

does the first degree injury• Remember, the endoneurial tube is

maintained in this level of injury

Third degree Injury

• Loss of organization of endoneurial tube, funiculi, and Wallerian Degeneration

• Regeneration is hampered by multiple things• These problems result in incomplete re-

innervation with permanent losses in some functions

• Recovery is longer than with second degree injuries

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• Hoffman-Tinels sign can be elicited, but due to the fact that the endoneurialtubes have been disrupted, it is found that the sensitisation of these fibers does not indicate that these fibers are regrowing in their original tubes

Fourth Degree Injuries

• The continuity of the nerve sheath is maintained, but is so disorganized that it eventually becomes a tangled mess of connective tissues

• All functions of the nerve are lost• Surgical repair is required with removal

of the effected segment, if any significant recovery is to occur

Grade 5 Injuries

• Loss of continuity of nerve trunk, thus a complete loss of all functions

• Scar tissue may form between the ends of the injured nerves

• Left untreated, recovery will not occur• Surgical correction is required

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• Brachial plexus injuries also occur, and are mostly due to tractional injuries

• When the arm is by the side, the upper part of the plexus is most susceptible to injury

• Thus, injuries that produce forced lateral flexion with the arm at the side affect the upper portions of the plexus first

• With an abducted arm at 90%, traction tends to damage all components of the plexus equally

• When the arm is hyperabducted, and the are is trationed, the lower parts of the plexus are damaged

• This type of injury is seen most often with forced lateral flexion of the head, such as concominant striking of the head and apex of shoulder following throwing of a patient off of motorcycle onto pavement

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• 3 main Thoracic Outlet Syndromes are classically described. These are the

• Sclanus Anticus Syndrome (or cervical rib)• Costoclavicular Syndrome• Hyperabduction Syndrome• The first of these has a predominance of

neurologic findings, whereas the latter two seem to exhibit more vascular findings due to the anatomic location of venous tissue

• Ganglioneuropathies - or Double Crush Syndromes - have been identified

• These seem to incorporate interference with axoplasmic flow as their causitive agent

• This predisposed distal neurologic sites to injury, and thus symptomatology

• Isolated peripheral nerves may also be damaged, and this damage must be differentiated from the formerly mentioned conditions

• Keeping this in mind, peripehral neuropathies or tunnel syndromes that show up in the periphery MAY be related to cervical spinal whiplash (CAD) injury

• Peripheral nervous system tissue the is susceptible may manifest initial or increased symptomatology if the appropriate pathologic stimulus is supplied to proximal aspects of the peripheral tissue

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Peripheral Neuropathies

• Compression or stretch of peripheral nerves effects the large myelinated fibers preferentially.

• Thus, there is a specific order of sensation loss/alteration with peripheral compressive events.

• The loss occur in the following order, and recovery occurs in exactly the reverse fashion:

Order of loss of Sensations

• Conscious proprioception and discriminative touch

• Cold• Fast pain• Heat • Slow Pain

• The previous description is for sensory modalities only, and does not encompass motor findings

• Motor axons for volitional motor activity are of the A alpha type

• Autonomic efferent fibers are of the small type C variety

• Given these facts, a compressive neuropathy would preferentially impact volitional motor activity, with potential sparing of the autonomic function of the distribution of the peripheral nerve

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Order of Loss of Motor Function

• Motor components are also located in the peripheral nerve

• Alpha motor neuron axons (alpha axons) present from neurons in the ventral horn of the spinal cord or brainstem

• Autonomic axons (C and a delta type) from neuronal cell bodies in the intermediolateralcell column, brainstem and sympathetic ganglion are also present

Autonomic Fibers

• Small diameter autonomic fibers are also present in the peripheral nerves

• These fibers are derived from smaller sized neurons in the interomediolateralcell column, paravertebral ganglia, or nuclei of the brainstem or peripheral ganglia

Autonomic (Sympathetic) Denervation

• Initial signs of peripheral neuropathy that include damage of the autonomic fibers cause an initial vasodilation, with associated increases in temperature in the effected region

• Additionally, the region will undergo the inability to sweat, piloerector tissue will be unable to respond to neurologic stimuli and trophic changes occur to the local skin

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• However, although denervated, the effectororgans of this system still has the ability to respond to non-neuronal stimuli

• This stimuli such as cold, etc will cause a drastic vasoconstriction in the distribution of the denervated region

• Also it is known that the amount of postganglionic sympathetic fibers found in peripheral nerves are greatest in nerve that have a cutaneous distribution of the hand and foot as opposed to more proximal regions of the extremities

• RSDS/Shoulder-Hand Syndrome or Regional Complex Pain Syndromes may develop following Cervical spinal injury

• These conditions tend to develop in stages due to their cause, and clinically observable signs

• These stages are classically described as follows:

• Stage 1 - Insidious pain onset, with edema, and maintained ROM

• Stage 2 - following 3-6 months, stiffness and flexion deformities follow the resolution of edema

• Stage 3 - after an additional 3-6 months (variable due to multiple factors) trophicchanges in the distribution occur, with continued contracture presence. Because autonomic distribution is greater in hand and foot than proximally in limb, these effects are seen greatest distally

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Post traumatic Headache - the Post Concussive Syndrome

• Headache is the 2nd most common complaint following MVA

• Headaches that are traumatic in nature may arise from direct cranial trauma, or from injury to the underlying neurlogic tissue from the brain

• Additionally, damage or changes in chemistry of injuries tissues may contribute

• Etiology Factors for Posttraumatic Headaches– Head contact - 57.3%– Whiplash 43.6%– Object (free object) hit head - 13.7%– Body was shaken - 9.4 %– Other 13.7%

• Recent studies have demonstrated a sensitization of the underlying trigeminal system that occurs following trauma

• This sensitization causes stimuli that may ordinarily be interpreted as normal to be inappropriately determined as being painful

• Also, this system may give rise to spontaneously generated action potentials that when present in a nociceptive system are interpreted as painful stimuli

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• However, even if damage to all the aforementioned tissues can generate headache conditions, due to the currently available studies it seems viable that other causes must be considered

• This is due to the finding of DAI (diffuse axonal injury) in MTBI (mild traumatic brain injury)

• This injury to axonal tissue of the CNS has been thought of as psychogenic in the past, however is well documented

• This injury has a range from small regions of axonal shear, to large regions of evident axonal injury

• Most often, the injury to these axons in non detectable on radiographs, CT, MRI, EEG, CSF evaluation, etc. (PET scans have shown promise in their diagnosis but are not currently the assessment tool of choice clinically)

Diffuse Axonal Injury

• Most common cause of vegitative state and severe disability following injury

• aka diffuse degeneration of white matter, shearing injury, diffuse damage of immediate impact type, diffuse white matter shearing injury, inner cerebral trauma

• Now DAI is the term

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Examples of DAI

• Three distinct findings in DAI– focal lesion in corpus callosum often involving the

septum and associated with intraventricularhemorrhage

– focal lesion in one or both dorsolateral quandrantsof rostral brainstem

– microscopic evidence of damage to axons

– First two may be identified – Third can only be identified histologically

• Multiple axon bulbs can be identified in acute injuries

• MC in parasagittal white matter, corpus callosum, IC, thalami and in ascending and descending tracts of stem

• Later, large numbers of small clusters of microglia can be seen throughout white matter of hemispheres and in brainstem

• Bulbs most effectively seen within 2 weeks of injury

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• Clinical course - these patients have lower incidence of lucid interval, fx, contusions, hematomas, and evidence of increased ICP, as compared with with patients without this injury

• Usually associated c MVA• Known to exist in varying degrees of severity,

and in a continuum from concussion up to persistent post-traumatic coma

• Grades of DAI• grade I - histologic evidence only throughout

white matter, no focal accentuation in CC or stem

• grade 2 - widely distributed axonal injury, and focal lesion in CC

• Grade 3 - most severe, and end spectrum of disorder, has diffuse damage to axons in presence of focal lesions in both CC and in stem

• It appears the mechanism is initial damage to axon at nodes of Ranvier where there is fragmentation of axolemma - called primary axotomy

• This is due to axonal shearing and resealing of fragmented axon within 60 minutes post injury

• With survival there is accumulation of transported axoplasm and organelles, This disrupts the axollema and undergoes secondary axotomy

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• Secondary axotomy is believed secondary to calcium influx that activates proteases that degrade membrane proteins and neurofilaments

• Another theory states that dirsuption of axonal transport results in mictotubularand neurofilamentous disturbances of cytoskeleton

Symptoms of PCS (DAI)• Lightheadedness, Vertigo, dizziness, neck

pain, headache, photophobia, phonophobia, tinnitus, impaired memory, easy distractibility, impaired comprehension, forgetfulness, impaired logical thought, difficulty with new or abstract concepts, insomnia, irritability, apathy, anger, mood swings, depression, loss of libido, pesonality changes, and intolerance to alcohol

Mild Cranial/Nervous Trauma

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Just Plain Ouch!

• Incidence of complaints in post traumatic headache patients– Headache 82.9%– Irritability 66.7%– Insomnia 63.2%– Anxiety 58.1%– Memory problems 57.3%– Other pain 56.4%– Concentration problems 52.1%– Depression 52.1%

– Dizziness 41.1%– Confusion 41.1%– Emotional changes 36.8%– Decreased libido 35.0%– Tinnitus 29.1%– Cannot carry out plans 29.1%– Cannot plan 28.4%– Flashbacks 28.2%– Do not enjoy sex 26.5%– Nightmares 26.5%– Arithmetic problems 17.9%

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Neurobiology of Diffuse Lesions

• Traumatic injury to the CNS primarily causes immediate mechanical disruption of neural pathways and vasculature and secondary neuronal or cellular damage that develops over a period of hours after initial traumatic insult

• Post traumatic neurochemical changes may involve alteration sni the synthesis or release of both endogenous neuroprotectivechemicals or autodestructive compounds

• Acetylcholine - elevated in CSF and brain post injury

• Some component of neurological distubancesand perhaps neuronal damage after TBI appear to be due to increased function of cholinergic systems located in brain regions (thalamic,amygdala, cingulofrontal cortex)

• Calcium homeostasis has been reported to be altered and underlie delayed neuronal death after subarachnoid hemorrhage and cerebral ischemia

• Increases in intracellular calcium can also activate calcium specific neutral proteases, which will cause profound cytoskeletaldegradation and neuronal death

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Post concussive syndromes• Criteria should include, duration of LOC of 30

minutes are less, or being dazed without loss, initial Glasgow Scale of 13 to 15 without deterioration , and absence of focal neurological deficits

• Loss of consciousness does not have to occur for the postconcussion syndrome to develop

• Authors have stated that up to 50% of patients with mild head injury will develop this

Postconcussive Syndrome

• Often diagnosed as “concussion,” or closed head injuries

• Can occur with or without direct head trauma

• Due to axonal shear, and this diffuse axonal injury is found to be created in side wihiplash motions more than rear impact motions

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• A 52 year old customer in a Home Depot Store in Florida suffered the following: Vertically stacked lumber fell, striking her on the top of her head. She had a small scalp laceration, but did not lose consciousness. She sued Home Depot for at least $100,000 for alleged brain damage and an unspecified amount for paranormal injury. She claimed that her mild head injury robbed her of a supernatural power - her ability to go on “automatic” - to undergo pain free surgery without anesthetic

• The broward circuit court jury of three men and three women awarded her with $5000 for physical injuries, but found that she was 80% negligent. They also awarded her husband $1000 for loss of her services

• The plaintiff stated “Welcome to the real world. People do not look beyond the normal, to what can be.”

• The patient claimed to be a psychic, but had not foreseen the outcome of her case, and if she had, she would not have pursued it.

• The patient and her husband rejects a settlement of $17,000, and insisted on more than 1 million dollars.

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• Headaches occur in 30-90% of mild head injury

• Dizziness and hearing loss occur in 53% of patients within 1 week of injury and persist in 18% after 2 years

• Labyrinthine concussion and vertigo may result, or benign positional vertigo may occur do to the settling of dislodged otoconia from urticular maculae onto cupula of the posterior semicircular canal

• Conductive hearing loss may occur secondary to bleeds, etc.

• Visual symptoms, blurred vision, after mild head injury occurs in 14% of patients

• convergence insufficiency is the most common cause

• Lesions of the occipital lobe and upper midbrain are possibilities

• Cognitive impairment is seen in patients - one study showed 19% had loss of memory and 21% had concentration difficulties

• Seizures, amnesia, and movement disorders may also occur

• This mild head injury has also been linked and suggested to be a factor that may lead to Alzheimer’s disease

• This may begin an inflammatory cascade that depositis B amyloid protein in areas, and that this can lead to initiation of Alzheimers like process

• SPECT scans can be used to study mild head trauma, and have shown decreased perfusion in the frontal and temporal lobes mainly

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• EEGs do not appear to high yield, other than for post traumatic seizure disorders

• Persistent symptoms -• HA - 1 month 33 to 90%, at 4 months

47-78%. At 4 years 24%• Dizziness - 25% at 1 year, and 18% at 2

years• Memory problems - 18% at 1 month,

59% at 3 months, 15% at 6 months, up to 25% at 1 year and 19% at 4 years

• Most patients seem to resolve by 3 to 6 months, however some persist

• Risks for persistent sequelae include >40 yoa, lower educational, intellectual and socioeconomic status, female gender, alcohol abuse, prior head injury, and multiple trauma

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Prognostic Expectations and Factors

• Keep in mind, the change in velocity of vehicles is important, but studies have shown in crash test dummies, the forces of over 11g have translated to the C spine from vehicles traveling as low as 15 mph

• This is in excess of 100 lb of force on the cervical spine

• Factors affecting outcome -• Age - between 0-16 years, the cord is at

damage (as is other parts of CNS), but few fractures are seen

• Flexibility and nitrogen balance may impact this

• > 60 yoa, osteoporosis predispose to fx, as well as spondylitic changes predisposing to cord injury

• Healing times of the elderly may be slower, as well as vasculopathies impacting healing

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• Spinal canal size may lead to disc herniationsand cervical myelopathy

• The more narrow the canal, the greater the risk for neurologic injury, as well as the greater the risk for future neurologic deficit

• Narrowed canals may be – congenital– hypertrophic posterior facets– ossified PLL– Discogenic spondylosis with buckling of

ligamentum flava– hyperlordosis

• DJD in the form of the following:• Enlarged facets may lead to radiculopahy due

to IVF encroachment, or canal encroachment• Does DJD follow trauma? One study has

shown a degenerative changes in 39% of post injury patients cervical spines, when only 6% of non injury patients exhibited this finding

• All patients were without DJD immediately post injury

• DJD was found in patients that had fixation on flexion and extension films, who had suffered unconsciousness, or or who wore cervical supports more than 12 months, and this DJD was found in 60% of patients

• Again these patients was normal at initial evaluation, and these findings were observed at the time of final evaluation

• DJD at time of injury also causes a poor prognostic outcome

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• An interesting finding is hypertrophic bone may impact IVF, canal, or transverse foramen

• This arises from joints of Luschka and posterior facets

• This combination typically caused cervicoradiculopathy - especially at C5/6

• With age the disc dehydrates, and this diminshed height predisposes to cord injury, and alters the biomechanics of the joint

• Adjacent levels are predisposed to advanced DJD changes and discopathy

• Disc degeneration may lead to osteophyteformation on posterior-inferior portion of vertebral body, and thus canal size may be impacted

• IVF size is diminished with disc degeneration• AS complicates injury, as pseudarthrosis is a

concern, as is muscle atrophy

• Hypermobility secondary to inflammatory arthritides such as RA are complicating factors

• 85% of C spine motion takes place in upper C spine, and dislocations are a concern with RA, as are odontoid erosiion, atlas subluxation, and increased ADI

• Blocking of vertebrae, surgical or congenital, are also complicating factors

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Croft Proposed Prognostic Scale

• Classified as major injury category (MIC)• MIC 1 - pts present with symptom srelating

directly to injury, with no objective findings of loss of motion, or neuro complaints - 10 points assigned to this level

• MIC 2 - presentation of decreased ROM of C spine in addition to MIC 1, but no neurologic deficits - 30 points assigned

• MIC 3 - MIC 1 and 2 upon presentation, along with objective signs of neurological loss (sensory or motor) - Interestingly, Dr. Croft suggests that these neurologic findings be verified by a neurologist - 90 points assigned

• When categorized in this fashion, one study showed that 56% of MIC 1, 81% in MIC 2, and 90% in MIC 3 had residual pain

• These were typically neck pain, headache and paresthesias

• It appears that groups 1 and 2 do well with conservative care, but group 3 present with neurologic signs and may or may not

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Modifiers as Proposed by Croft

• These conditions compound or alter the prognosis and are given numerical values as are the MIC classifications

• Canal size of 10-12 mm - 20 points• Canal size of 13-15 mm - 15 points• Straight cervical spine - 15 points• Kyphotic cervical curve - 15 points• Fixated segments - 15 points

• Pre-existing DJD - 10 points• Loss of consciousness - 10 points• These modifiers are cumulative, with

the exception of canal size, and curve• Prognostic Groups

Prognostic Groups

• Group 1 - 10-30 points – This group has an excellent prognosis, and no

objective findings are expected.– Residual findings, if present, will usually be

confined to mild muscle pain, and occipital headaches, and intermittent stiffness

– Many recover fully, and no reasonable chance for develop medication dependence, neuro deficits, or need surgical intervention

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• Group 2 - 35-70 points– This group has a good prognosis, and

neuro deficits, surgical intervention, and medication dependence are unlikely

– Expected residuals include intermittent pain, stiffness and potentially headache

• Group 3 - 75-100 points– Prognosis for this group is fair, and neurologic

symptom development may occur– Residual symptoms may include numbness, or

even weakness– Surgical interventions, dependence on meds, or

surgical intervention probability is still low– Second opinions in this case are listed as being

“reasonable”

• Group 4 105-125 points – Probability of future or persistent

neurological deficits is likely– Prognosis is listed as poor– Future symptoms may include weakness,

atrophy, radiculitis, etc. and surgical intervention may be necessary in the future

– Second opinions are warranted

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• Groups 5 - 130-165 points– This represents a clinical picture prone to

deterioration – Prognosis may be listed as unstable, or just bad– This condition has a poor likelihood of responding

effectively to conservative care– The patient will probably require surgical

intervention, and thus has a good likelihood of requiring medication and having continued neurologic symptoms

THANK YOU!!

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How does the subluxationcomplex effect our system?

• It has been seen that certain areas of the spines in humans are said to be “facilitated.”– that is, they show an increase in neurologic

activity with minimal stimuli, and this increased response has been noted to be present for a period of months-

– This facilitation is believed associated with the subluxation complex

• Chronic c fiber activation and volume transmission

• Diffuse nature of neurotransmitter • Increased activity in dorsal, ventral and lateral

horns• Effects of gamma, alpha motor neurons, and

the interomediolateral cell column• Heightened sympathetic activity or

“sympatheticotonia.”

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• It is believed that both the motor and the autonomic function are affected in this zone of segmental facilitation– this includes the anterior and lateral horn cells,

and ascending pain pathway cells– Thus, the neuronal response to all stimuli (from

the body and from the brain) is heightened– Afferents arising in the viscera or adjacent

musculoskeletal system may be involved in this process of facilitation (ie - the coffee response)

• How could the muscular system contribute to this facilitation?– It is possible that based upon the spindle gain of

the muscle set by the brain, physical changes may lead to the subluxation complex via

• approximation of articulations, with decreased spindle afferent firing, resulting in increased descending gain, allowing for increased spindle sensitivity, and thus increased extrafusal muscle tone

• Joint surfaces approximate with limited motion and potential inflammation

• Gravity and postural reflexes accentuate the sensitized spindle extrafusal muscle tone

• This increase in the central and peripheral inputs to the segment would create facilitation at this level– This also could be affected by increased or

altered input from joint proprioceptors at a segmental level - ie inflammation with increased afferent bombardment at that level

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• How would adjustments potentially effect this?– Research has shown that the transversospinalis

group of deep back muscles (spinalis, multifidusand rotatores muscles) as well as the longus colliand longus capitis muscles differ from other muscles due to their large comparative density of muscle spindle receptors

– These muscles (especially the transversospinalismuscles) are therefore believed to have an extremely important role in advising the CNS of proprioceptive and muscular stretch information

– It is believed that this large number of afferents, when depolarized, would alter the descending barrage of gamma motor neuronal activity, reducing its magnitude

– Additionally, the capsule of the synovialzygopophyseal joints is important

• capsule is highly innervated from medial branch of dorsal primary ramus at level of joint and each level above and below

• In capsule are 3 types of sensory receptors• Type I - static and dynamic mechanoreceptors with

continual firing• Type II - less sensitive mechanoreceptors only firing with

movement• Type IV slow conducting nociceptors

• Stimulation of these mechanoreceptors has been shown to normalize muscular tone on both sides of the joint (again, recall the three level innervation of these segments)

• Additionally, the counter-irritant, or gait theory would allow for these large diameter afferents to in effect decrease the frequency of firing of small diameter nociceptive afferents at the segment, thus decreasing the facilitation at that level

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• Also, stimulation of the golgi tendon organ of the musculotendinous junction would allow for decreased frequency of firing of the ventral horn cell to the extrafusal muscle fibers, as well as decreased firing of the gamma motor neuron to the muscle spindle

• Normalization of mechanics of the articulation is gained, with attendant decreases in excessive spindle and extrafusal muscular activity

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