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					Serious and Unusual Damage from Whiplash Injuries

Serious and Unusual Injuries from MVAs

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45 years old female, left side swipe MVA. 10 days in hospital for concussion and distorsion of the neck and discharged in a soft collar PT for “muscle relaxation. She underwent physical therapy focussed on the relaxation of muscles in the region of the cervical spine.
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Pain persisted and 6 weeks later she was re-examined and a cock robin deformity was noted Lateral X-rays were –ve for ADI

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Other views and CT demonstrated a Grade 1 AARF of C1/2 One year after the MVA fusion of C1/2 was performed for worening pain

Stulik, J. Krbec, M. Atlanto-axial rotation dislocation (case report)] Acta Chir Orthop Traumatol Cech 69:1 49-53 AtlantoTraumatol 492002

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Definitions
Whiplash, as a term, was first used by HE Crowe at the 1928 Annual Meeting of the Western Orthopedic Association. “.. an acceleration-deceleration mechanism of energy transfer to the neck ..”
QTF 1995

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Mechanism of Neck Injury
Classical Lordosis Compression/extension

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Compression/Extension
1. Impact 2. Acceleration of target vehicle 3. Seat contact with body 4. Simultaneous forward and upward movement of occupant 5. Extension and compression of the lower Cspine 6. Flexion and compression of the upper Cspine
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Sequence of Events Summary
7. Formation of the S-curve 8. Cspine extension and posterior head rotation 9. Head contact with head rest 10.Forward acceleration of the head past the shoulders 11.Flexion of the complete Cspine
• Kaneoka, K, et al. The mechanism of zygapophyseal joint injury in rear end motor vehicle collisions. J Jap Spine Res Soc 8:244 1997

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Effects of Current Version
While the classical effects do have a role the overall effect is much more complicated. New effects include: Compression Anterior shear Abnormal extension Wider separation of the anterior column Closer approximation of the posterior column
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Effects of Current Version
In total, a complete departure from normal daily perturbations and even from other hyperextension injuries. Therefore there is no reason to expect the injuries caused by whiplash to be similar Therefore is no reason to expect this injury to respond to rest and treatment in the same way that that superficially injuries similar do.
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Damage
Brainstem Cerebral Spinal Cord Labyrinth Arterial Musculoskeletal
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Brain Stem

Brain Stem
Structures of Interest •Cranial Nuclei and Nerves •Long Tracts •Descending Sympathetic Nerve
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Brain Stem
Damage
Concussion Contusion/ Laceration Petechial Hemorrhage Ischemia Congenital predisposition Infarction

Brainstem Contusion
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Brain Stem
Characteristics
upper motor neuron signs hemilateral signs and symptoms cranial nerve signs and symptoms long tract signs and symptoms Horner’s syndrome

Brain Stem
Evaluation Descending Sympathetic Nerve Examination Long Tract Examination Cranial Nerve Examination

Horner’s Syndrome
ptosis miosis anhydrosis enophthalamus Erythema (facial reddening )
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Horner’s Syndrome

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Horner’s Syndrome
Miosis and ptosis of the left eye

Dilation of right eye after infiltration of cocaine solution
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Long Tract Examination
Light Touch Pinprick ( or thermal) Deep Tendon Reflexes Hoffmann’s Babinski (Oppenheimer) Vibration Proprioception (Postural and Kinesthesia) Strength Spasticity
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Cranial Nerve Examination
CN 1 Symptoms Anosmia paraosmia (more common) Hemianopia quadranopia Test Smell ID Positive Unable to identify common smell

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Confrontation

Bilateral hemianopia or quadranopia Paresis, paralysis, nystagmus, Sluggish, absent or oscillating response

Diplopia, pupil Tracking, dilation, consensual torticollis, reflex strabismus, photophobia

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Cranial Nerve Examination
CN 4 Symptoms Diplopia, torticollis, strabismus, Facial parasthesia, Dysgeusia Diplopia, torticollis, strabismus, Facial Asymmetry Dysgeusia Hyperacusia Test Tracking Positive Paresis, paralysis, nystagmus,

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Sensation Jaw reflex Jaw Clonus Tracking

Hypo or anesthesia Hyperreflexia Clonus Paresis, paralysis, nystagmus,

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Smile-Frown

Smile lost- frown retained Smile and frown lost
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Cranial Nerve Examination
CN 8 Symptoms Dizziness Blurred vision Hypacusia Tinnitus Dysphagia Dysgeusia Dysphonia Test Body Tilt Finger rustlehum Gag (not done) Laryngoscope Positive Dizziness Hypoacusia-hum in deaf ear Hypoacusia-hum in good ear N/A Vocal cord paresis or paralysis

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Cranial Nerve Examination

CN 11

Symptoms Dysphagia

Test Phonation Trapezius strength, reflex, clonus, Shimizu Tongue protrusion

Positive Uvular deviation Weakness, hyperreflexia, clonus Abduction of shoulders &/or shoulder girdle elevation Tongue deviation

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Dysarthria

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Visual Tracts

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Edinger-Westphal Pupil Changes & Light Reflexes

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Oculomotor - Levator Palpabrae
Ptosis

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Extra-ocular Muscles

Primary Gaze Position- Strabismus
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Extra-ocular Muscle Paralysis

Left Gaze
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Extra-ocular Muscle Paralysis

Right Gaze
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Right Lateral Rectus Palsy

Right Gaze

Primary Gaze

Left Gaze
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Right 3rd. Nerve Palsy

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Facial Nerve

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Vagus
Phonation Uvulae and Soft Palate Deviate Towards Strong Side Dysphagia Dysphonia

Symptoms

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Hypoglossal

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Head Injuries
MVAs cause 136,000 head injuries annually MVAs cause 42% of all head injuries MVAs cause 40% of all CNS trauma 50% of all MVA patients have abnormal EEGs

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Cerebrum – Concussion
Definition for this course A usually reversible traumatic paralysis of nervous function following violent shaking and agitation of the brain,

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Cerebrum – Concussion
Characteristics •Loss of conciousness •Always loss of memory •Either a direct blow or contracoupe as cause
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Traumatic Brain Injury
?? 25% of Whiplash Patients Affected
MILD Any period of loss of consciousness <30’ Any loss of memory for events immediately before or after the accident <24 hours Any alteration in mental state at the time of the accident (e.g., feeling dazed, disoriented, or confused) Focal neurological deficit(s) that may or may not be transient

Traumatic Brain Injury
Evaluation - Subjective
Did you hit your head Were you knocked out How is your memory Do you have fainting spells Do you have blackouts How is you concentration Do you get drowsier than prior to the accident

Traumatic Brain Injury
Evaluation - Subjective
Are you having difficulty reading Are you having trouble complying with or understanding instructions Is the problem getting worse Ask them about their condition, its prognosis and treatment as it was explained to them by you previously Ask the patient’s partner Is there anything along these lines that you want to tell me

Traumatic Brain Injury
Evaluation - Objective
Ask the patient to remember 3 unassociated items Ask the patient to demonstrate exercises Ask the patient to repeat instructions Neuropsychological Evaluation

Traumatic Brain Injury
Our Concerns Patient’s well being Compliance

Traumatic Brain Injury
Management
Refer to Physician Accommodate Problems clear precise instructions written instructions shorter exercise programs reiteration more one to one time instruct partner simultaneously

Intracranial Pathology
Intracranial Bleeding and Hydrocephalus
While most catastrophic intracranial bleeds are quite rapid, with the crisis occurring within 24 hours of the injury, some are much slower taking many days or even weeks to build up the crisis, which is generally quite sudden taking the form of a stroke, coma or death. Cervicogenic headaches are generally not progressive and are usually very different in quality and location to that of the

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Headache May occur when lying flat May awaken patient from sleep May increase with change in position May increase with bending, straining, and coughing Nausea, vomiting Change in alertness (level of consciousness) Apathetic, withdrawn Sleepy, lethargic

Symptoms

Brainstem signs and symptoms Difficulty writing or reading Weakness Movement difficutly Loss of fine motor skills Hand tremor Loss of coordination Dysequilibrium Seizures

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Among clinical indications that a bleed or hydrocephalus may be occurring are: Headaches a that are deep, dull, diffuse, and boring in nature Sudden severe+++ headache (epidural) Progressive headaches Intellectual impairment such as drowsiness, concentration and memory difficulties

Spinal Cord

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Spinal Cord
Damage Compression Hemorrhage Tumor

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http://www.amershamhealth.com/index3.shtml

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http://www.amershamhealth.com/index3.shtml

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Spinal Cord
Characteristics
bilateral or quadrilateral or trilateral distribution upper motor neuron signs spasticity hyperreflexia clonus hypoesthesia paresis paraesthesia
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Spinal Cord
Evaluation
deep tendon reflexes (hyperreflexia sensation (hypoesthesia clonus (clonus) strength (paretic) rapid passive movement (spasticity) extensor-planta or Oppenheimer test (Babinski response) Hoffmann’s Test (Flexor withdrawal response)
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Spinal Cord
Evaluation
Best current evidence is that the most sensitive test for cervical spinal cord lesions is Hoffmann’s test.
Sung, RD. Wang, JC. Correlation between a positive Hoffmann’s reflex and cervical pathology in asymptomatic individuals. Spine 26(1):67-70 2001

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Labyrinthine Concussion

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Labyrinthine Concussion
Cupulolithiasis Canalolithiasis Tympanic Membrane Rupture Oscicle Fracture/Dislocation Perilymph Fistula Traumatic Hydrops Temporal Fracture
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Oscicular Fracture/ Dislocation

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Tympanic Membrane Rupture
Usually caused by sharp pressure changes, otitis media or direct trauma (sticking things in the ear).

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Tympanic Membrane Rupture and Fracture/Dislocation of the Oscicles
History •Otalgia •Conduction Hearing Loss •Pressure induced (alternobaric) vertigo •Sound induced vertigo (Tullio’s phenomenon)

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Tympanic Membrane Rupture and Fracture/Dislocation of the Oscicles
Objective

•Clinical Hearing test (conduction loss) •Hennebert’s test •Otoscopy

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Perilymph Fistula

An opening usually between the inner and middle ear through the round or oval window

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Perilymph Fistula
History: •Sensorineural hearing loss that may be constant or fluctuating •Aural fullness •BPPV and Dysequilibrium •Pressure and sound induced vertigo •Exercise induced vertigo •Motion intolerance •Nausea and vomiting •Tinnitus •Otalgia
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Perilymph Fistula
Objective:

•Vestibular tests (Body tilt, Hallpike-Dix etc) positive •Romberg or tandem (sharpened) Romberg may be positive. •Positional nystagmus •Sensorineural hearing loss •Hennebert’s sign

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Traumatic Hydrops
Excessive build up of fluid in the membranous labyrinth.

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Traumatic Hydrops Causes Reaction to direct membranous labyrinth injury Injury to the endolymphatic drainage system
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Traumatic Hydrops History Delayed onset of vertigo Non-positional vertigo or BBPV

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Traumatic Hydrops Objective Body-tilt test Hallpike-Dix test

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Temporal Fracture
Longitudinal, transverse and mixed. Longitudinal fractures caused by blows to the occipital or frontal regions. Both types can extend through the middle and/or inner ear.
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Temporal Fracture
History Direct blow Temporal pain Hearing Loss (sensorineural, conduction or mixed) Tinnitus Vertigo BPPV (from associated other labyrinthine concussion causing perilymph fistula and otoconic displacement)

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Temporal Fracture
Objective Battle Sign when through the petrosal bone

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Neurovascular

Carotid Artery Vertebral Artery

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Anatomy

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Traumatic Pathologies
Intimal and media tearing (intramural tears) Pseudoanurysm Dissection/Transection arteriovenous fistulae Thromboembolus Bruising/ Atheroma Vasospasm Collar hematoma
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Carotid Artery

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Carotid Artery
Most common at the internal carotid artery near the base of the skull. Type 2 injuries are those caused by MVAs and occur high at the angle of the jaw and the upper transverse processes. The backward-forward movement of the brain stretches the artery and may bring it against the bony structures.
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Most common at the internal carotid artery near the base of the skull. Type 2 injuries are those caused by MVAs and occur high at the angle of the jaw and the upper transverse processes. The backward-forward movement of the brain stretches the artery and may bring it against the bony structures.

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Symptoms are usually delayed sometimes for months. They include: Common Hemicrania (unilateral headache) Loss of temporal artery pulse (only in injury to the common carotid artery) Moderately Common Aphasia Horner's syndrome (eyelid ptosis, miosis, and unilateral anhidrosis) Transient ischemic attack Rare Bruit Hemiparesis in alert patients Neck hematoma Unilateral facial weakness
http://www.physsportsmed.com/issues/1996/02_96/troop.htm 100

Vertebral Artery
These are more likely to cause strokes than carotid artery injuries and are more likely to be adversely affected by therapy. The number of anomalies that commonly affect the vertebrobasilar system leave it vulnerable
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Right Hyoplasia

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FMD

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Basilar Aneurysm and Absent R. Artery

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Stenosis Near Origin

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Characteristics
Main Signs/Symptoms
•Dizziness •Posterior Headache •Changing Cranial Nerves Signs and Symptoms

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Transverse Process Fractures and the Vertebral Artery

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Transverse process fractures were present in 24% of 216 patients with cervical fractures In 78% the fracture extended into the transverse foramen. Dissection or occlusion of the vertebral artery occurred 88% of the patients undergoing angiography Two of these had clinical evidence of vertebralbasilar artery stroke. Vertebral angiography should be considered when patients with transverse process fractures extending into the transverse foramen develop signs and symptoms of vertebral-basilar artery insufficiency.
Woodring, JH. Lee, C. Duncan, V. J Trauma. Transverse process fractures of the cervical vertebrae: are they fractures insignificant? 1993 Jun;34(6):797-802. Jun;34(6):797-

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Dizziness Definitions
Dizziness: a sensation of dysequilibrium. Vertigo: an illusion of spinning. Oscillopsia: an illusion of linear or swinging motion Central dizziness: that caused by neurological compromise Peripheral dizziness: that from causes other than neurological
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Symptom Based Classification
Type 1 Vertigo or Oscillopsia Type 2 Pre-syncope Type 3 Dysequilibrium

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Central v Peripheral Vertigo
Central Persistent Milder May alternate (PAN) Assoc. nystagmus may be purely linear Assoc. nystagmus may alternate Assoc. nystagmus gaze evoked Other neurological signs Peripheral Non-persistent Profound if labyrinthine Constant direction Assoc. nystagmus is curvilinear Assoc. nystagmus constant in direction Assoc. nystagmus gaze suppressed No other neurological signs
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Evaluation: Subjective
Associated or disassociate dizziness, headache and neck pain. Did they occur at the same time Do they vary with each other in intensity Are they exacerbated and relieved by the same mechanisms Do they progress with each other Are the headache and dizziness associated but both are disassociated from the neck pain
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Evaluation: Subjective
What brings on the symptoms What are the quality of the symptoms Are any of the pains neuropathic Is there parasthesia What type of dizziness is experienced How long does the dizziness last How severe is the dizziness
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Evaluation: Subjective
Visual field disturbances Diplopia Facial parasthesia Dysgeusia Hyperacusia Dizziness Hypoacusia Tinnitus
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Evaluation: Subjective
Dysphagia Dysphonia Dysarthria Drop Attacks Perioral Parasthesia/Hypoesthesia Dysphasia Posterior Headaches Cape distribution of Parasthesia
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Evaluation: Observation
Horner’s Syndrome Facial flushing Ptosis Miosis Enopthalamus Anhydrosis Ataxia
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When Not Examine
After TP # with no angiography Facet dislocation Headache and dizziness mutually associated but dissociated from the neck pain Neurological S/S associated with dizziness or head movements Undiagnosed non-segmental neurological S/S
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Evaluation: Clinical Objective Tests

Carotid Pulses de Kleyn Minimized de Kleyn Progressive Minimized de Klyen Hautard’s
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Evaluation: Clinical Objective Tests
Minimized Hautard’s Hallpike-Dix Minimized Hallpike-Dix Cranial Nerve While Symptomatic

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Evaluation: Clinical Objective Tests
Reproduction Tests Differentiation Tests

de Kleyn Minimized de Kleyn Progressive Minimized de Kleyn Hallpike-Dix Minimize Hallpike-DIx

Cranial Nerve Exam Body Tilt Body Rotation Hautard's

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Pros and Cons to Testing
Pros May demonstrate + Peer behavoir Little or no risk Why not Cons Sensitivity/ specificity unknown May take some time May produce discomfort and vasovagal effects May cause overconfidence in negative results
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Evaluation: Clinical Objective Tests

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Evaluation: Imaging Tests

Digital Subtraction Angiogram Contrast Angiogram Magnetic Resonance Angiogram Doppler
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Digital Subtraction Angiography

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Transcranial Color Coded Duplex Sonography

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Comparison with angiography When compared to contrast angiography, transcranial Doppler ultrasound accuracy varies with the technical difficulty typically encountered in imaging any particular segment. The middle cerebral artery stem (M1 segment) is relatively easy to study, so ultrasound has a sensitivity and specificity of 9099% for finding a stenosis or an occlusion.10 For the more difficult to image intracranial (V4) segment of the vertebral arteries and the basilar artery, ultrasound has a sensitivity of 70-80% and a specificity of 90-99%.10,11 The accuracy of transcranial colour-coded duplex ultrasound is similar to that of contrast angiography. In a study of 310 patients, transcranial colour-coded duplex correctly identified 31 who had a stenosis of 50% or greater (confirmed by digital subtraction X-ray angiography).12 As all the stenoses were correctly diagnosed as true positives the sensitivity is 100%, but the specificity is 99% because one artery with a stenosis of less than 50% was incorrectly classified as having a stenosis of more than 50% (false positive). Comparison with magnetic resonance angiography (MRA) Intracranial MRA has a reasonable accuracy in comparison to contrast angiography for intracranial stenoses.13 The studies to date also suggest a good correlation between MRA and transcranial colour-coded duplex for imaging a stenosis or occlusion. In the anterior circulation arterial segments, transcranial colour-coded duplex has an estimated sensitivity of 75% and specificity of 99%, while in the posterior circulation, the sensitivity is 88% and the specificity 99%.14
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MRA

CEMRA

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CEMRA vs DSA
The sensitivity and specificity of MRA for detection of disease in the entire carotid and vertebrobasilar systems were 90% and 97%, respectively; for the carotid system alone, the sensitivity and specificity were 94% and 97%, respectively; and for the vertebrobasilar system they were 88% and 98% respectively. The overall interobserver reliability was 98% ( = 0.92).
Carina W. Yang et al. Contrast-Enhanced MR Angiography of the Carotid and Vertebrobasilar CirculationsAJNR 26:2095-2101, September 2005

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The 13 Ds
dizziness dysarthria dysphasia drop attack dysphonia dysphagia diplopia disequilibrium dystonia dysreflexia disequilibrium dysmetria dysunderstandingdys

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Damage
Rim Lesions A traumatic horizontal tear near the the disc, end-plate, centrum junctions

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Damage

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Damage

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Damage

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Damage

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Clinical Indicators of Severe M/S Damage
Sudden onset of severe pain (within 2 hours) Immediate loss of function Immediate torticollis Step deformity Severe+ movement loss Severe pain with mild compression Painful weakness on isometric testing Battle’s sign or Raccoon eyes
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Dislocated (Jumped) Facet
• The mechanism is hyperflexion and rotation. Only possible if the corresponding interspinous ligament and the joint capsule of the affected facet is completely ruptured. Can occur with only mininmal damage to the annulus fibrosus and the PLL. When the superior facet over-rides the inferior facet, this is termed a 'unilateral locked facet'. • Dislocation in the saggital plane is less than 1/2 of the anteroposterior dimension of the vertebral body. • About 25% have associated nerve root injury, and 25% have incomplete SCI.

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Bilateral Jumped Facets

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Flexion Teardrop #

Extesnion Teardrop #
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Jefferson Fracture

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Jefferson Fracture

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Dens Fracture

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Hangman’s Fracture

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Nexus Low Risk Criteria (NLRC)
• • • • • No posterior midline tenderness No evidence of intoxication Normal level of alertness No focal neurological deficit No painful distracting injuries

Only if the patient does not demonstrates any of the above should an X-ray not be ordered.
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Canadian C-spine Rules (CCR)
1. 2. 3.

4.

Age > 65 years Paraesthesia in extremities Dangerous mechanism of injury Fall > 3 feet (1 meter) Fall down > 4 stairs High speed MVA (>60mph or 100Kph) Axial load to head Rollover or ejection Collision with RV or bus Bicycle collision Car pushed into oncoming traffic Immediate onset of pain

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NEXUS V CCSPINERULE
Nexus 90.7% 36.8% Less useful later CCSpineRule 99.4% 45.1% More useful later

Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med 2003;349:2510-8. 163

Any High Risk Factor e.g. Age >65 Dangerous Mechanism Parasthesia in the Extremities Fragile Bone
Yes No

Low Risk Factors Simple Injury Ambulatory Delayed Onset of Pain Absence of Midline Tenderness
Yes

No

Radiography

Active Rotation > 45 degrees in Both Directions
Yes

No

Radiography Unnecessary

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Fractures
Tests Active movement Compression Isometrics Tuning fork These should not be carried out if there is strong evidence of a fracture.

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Fractures
Positives Severe multidirection restriction or no ROM Severe pain with light compression Painful weakness Pain
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Basal Fracture

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Medullary cranial nerve compromise CN 9-12 Headache

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Raccoon Mask

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Battle Sign

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Craniovertebral Instability

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Atlanto-axial Anterior Instability/Subluxation

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A/A Instability
Management Flexion and extension X-ray Blood tests No direct treatment

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headaches loss of pain / touch sensation over the trigeminal nerve distribution sleep apnea; down beat nystagmus facial diplegia; dysphagia (due to CN IX dysfunction);
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Atlanto-axial Fixation
Classification of axial rotatory fixation (AARF) (after Fielding) a. Type I: AARF without anterior displacement of C1. b. Type 2: AARF with 3–5 mm of anterior displacement of C1 on C2. c. Type 3: AARF with greater than 5 mm anterior displacement of C1 on C2. d. Type 4: AARF with posterior displacement of C1 on C2. (Reproduced with permission from JBJS 1977 Vol 59-A:No. 1. 'Atlanto-axial rotatory fixation' Fielding JW, Hawkins RJ).
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Type 1

Type 2 Type 4

Type 3

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Atlanto-axial Fixation

AARF Type 3
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Mainly young children (80%+) Usually associated with underlying pathology Usually relatively minor forces involved Fixed torticollis (cock robin deformity)

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Alar Ligament Tears
•Well established as a result of MVAs •There was no correlation between the MRI diagnosis of alar ligament injury and rotational or lateral shift of the atlas on plain X-rays.

Krakenes, J. et al. MRI assessment of the alar ligaments in the late stages of whiplash injury – study of structural abnormalities and observer agreement. Neuroradiol. 44:617-624, 2002

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Alar Ligament Tears
Common with long term Grade 2 WAD Occur mainly at the occipital attachment Less commonly at the dens Never in the body of the ligament

Krakenes, J. et al. MRI assessment of the alar ligaments in the late stages of whiplash injury – study of structural abnormalities and observer agreement. Neuroradiol. 44:617-624, 2002

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Alar Ligament Tears

History •Sub-occipital and occipital headaches •Type 2 dizziness

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Alar Ligament Tears

Tests •Kinetic •Stress

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Alar Ligament Tears

Positives •Delayed movement of the spinous process •Movement and soft capsule end feel

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Alar Ligament Tears

Management •Hard Collar 8-12 weeks •Stabilization Therapy

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Signs and Symptoms
+/-Neck pain + Sharp-Purser Test +/- Spinal cord signs and/or symptoms

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