Cervicogenic Dizziness - American Physical Therapy Association

5/2/2016
Speaker Information
• Daniel Maddox, PT, DPT, ATC, OCS, FAAOMPT
• OMPT Fellowship Director, Benchmark Rehab Institute
Cervicogenic Dizziness
Clinical Reasoning and Evidence
Related to Manual Therapy and
Exercise Management
• Hannah Norton, PT, DPT, OCS, FAAOMPT
• Assistant Professor & DCE, South College DPT Program
• Elizabeth Lane, PT, DPT, OCS, FAAOMPT
• Orthopaedic Residency Director, Benchmark Rehab Institute
• Derek Clewley, PT, DPT, OCS, FAAOMPT
• Assistant Professor, Duke University DPT Program
APTA NEXT: June 10th, 2016
*Disclosures Statement: For all speakers, no relevant financial relationships
or potential conflicts of interest exist.
“A Diagnosis of Exclusion”
Vestibular Review
Review of and Screening for Competing Hypotheses
Basic Anatomy
Inner Ear Anatomy
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Semicircular Canal Anatomy
Canal Orientation
Cupula Anatomy
Role of Canals, Utricle, Saccule
• Saccule
• Linear motion (up and down)
• Utricle
• Linear motion (fwd / bkwd and side to side)
• Canals
• Angular acceleration
• Push pull concept
• Each side has a match contralaterally that inhibits if ipsilateral
side excited
Translation of Information
• Signals travel along vestibular nerve to the brain
• Compares visual and somatosensory signals
• Determines position of head in space
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The Processing
Processing Abnormality = Nystagmus
www.ent-orl.com
• Afferent transmissions to vestibular nuclei
• Project to motor nuclei in brainstem, upper spinal cord,
cerebellum and thalamus
• Control of vestibulo-ocular-reflexes (VOR)
• Connects vestibular with occulomotor, trochlear, and abducens nuclei
Nystagmus
www.ent-orl.com
Nystagmus
• Named for the fast component
• Driven by slow component
• Usually fast component toward intact side
• (wheelchair example)
• According to the patient
• Pure upbeat, downbeat, right or left beat, or
torsional beat
• Mixed upbeat / downbeat with torsional
Peripheral causes of nystagmus
Peripheral Causes cont.
• Horizontal canal
• Anterior canal
• Pure horizontal
• Geotropic
• Beats toward earth
• Canalithiasis (BPPV)
• Ageotropic
• Beats away from earth
• Cupulolithiasis
• Torsional and DOWNBEAT
• Torsion direction is side of lesion
• Posterior canal
• Torsional and UPBEAT
• Torsion direction is side of lesion
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Peripheral Causes cont.
• Unilateral vestibular loss / hypofunction (UVL)
• (vest neuritis, acoustic neuroma / vestibular
schwanoma)
• Quick phase of nystagmusbeats away from intact side
• Acute – spontaneous, gaze evoked, head shaking
• Chronic – head shaking (with video lenses)
Central Causes of Nystagmus
• Usually pure upbeat, downbeat, rotational
• TIA / CVA
• Treatment – refer if first to detect
• Bilateral vestibular loss / hypofunction (BVL)
• Same as UVL if asymmetrical
• Otherwise if equal loss then only picked up with head
thrusts
• Otherwise treat the symptoms (balance, fall
prevention, gait, etc.)
Saccades
• CNS response to regain image
• Intact side drives the saccade
Other Differential
Hypotheses?
A Review of Related Anatomy
and Function
Cervicogenic Dizziness
Mechanisms
Daniel Maddox
• Cervical spine = A LOT of mobility, but at the
sake of mechanical stability1
• A highly intricate proprioception and motor
control system is required
• The neck is the link between the body and the
head, and must therefore be utilized to link the
two, requiring coordination with multiple
systems.
• Functional ramifications are many:
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A Review of Related Anatomy
and Function
Somatosensory System
Review
•For our purposes today
•Somotosensory
•Vestibular
•Visual
• Information arising from the periphery leads to
perceptions of proprioception, touch,
temperature, etc…2-3
• The proprioceptive system of the neck in
particular thought to be very developed, with
rich numbers of mechanoreceptors
• Especially muscle spindles, and especially in
the upper segments4
• Kristjansson and colleauges: The muscle
spindle afferents play “1st violin”! 5
Somatosensory System
Review
Vestibular System Review
• All of this afferent information provides the
CNS with info regarding where the head is in
relation to the body
• Utricle and Saccule:
linear acceleration,
gravity, and head tilt
• In addition, somatosensory afferents have
direct connections to the vestibular and visual
systems
• Semicircular Ducts:
angular acceleration
or rotation
• True for the C-spine ONLY5
Vestibular System Review
Visual Input
• Input ultimately primarily travels to the
vestibular nuclear complex (VNC) and the
cerebellum 6-7
• Processed along with visual and
somatosensory input at both.
• Efferents from the VNC project to neural
structures that control extraocular
muscles, cervical spine movements,
posture, balance, and ultimately higher
cortical areas 6,8
• Visual info is an important cue for motion
• No vestibular information from movement
at a constant velocity. Our sense of selfmotion relies entirely on visual input 9
• Visual illusions alone can stimulate a
sense of motion (Example: stationary and
nearby moving train)
• Visual input is processed with vestibular
and somatosensory in the VNC &
cerebellum
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Somatosensory Input
• Visual and vestibular input alone would
produce false information. Proprioceptive
input is needed to integrate and produce a
true sense of the body’s position in space 10
• Proprioceptive afferents are largely
dependent on the spindle-rich deep
intervertebral neck muscles 10
• Proprioceptive signals reach the VNC via
dorsal root axons, 2nd-order neurons, and
projections from cerebellar and cortical areas6
Somatosensory Input
• 3 relevant reflexes 4-5,11:
• Cervicocollic Reflex (CCR): mm’s react in response
to stretch to help stabilize head on body
• Cervicoocular Reflex (COR): thought to
complement the VOR to stabilize vision, and may
play larger role in the presence of vestibular loss
• Tonic Neck Reflex (TNR): thought to integrate
with the VSR to maintain postural stability via
changes in limb mm activity with body movement
relative to the head.
Cervicogenic Dizziness:
A Controversial Phenomenon
Cervicogenic Dizziness:
A Controversial Phenomenon
• First described in 1955 by Ryan & Cope as
“cervicogenic vertigo” 12
• Definition: “a non-specific sensation of altered
orientation in space and disequilibrium originating
from afferent activity from the neck” 13
• Rarely presents with true vertigo13-15
• Typically presents as unsteadiness, ataxia, or
postural imbalance in conjunction w/ neck pain,
stiffness, or HA 13
• Often other explanations for the symptoms exist,
and must be ruled out first 10
• Difficult to isolate CGD due to the many complex
interrelationships between vestibular input,
proprioceptive input, visual input, and central
processing.
• Lack of a specific diagnostic test
• How to explain some patients with severe neck
pain with no dizziness, and vice-versa?
Proposed Mechanistic Theories
Proposed Mechanistic Theories
• Neuro-Vascular Hypothesis or Posterior Cervical
Sympathetic Hypothesis
• Initially proposed by Barre’ in 1926
• Proposed that irritation of the cervical
sympathetic plexus could result in
vasoconstriction of the vertebrobasilar system
and subsequently the internal auditory
artery7,16
• No evidence has substantiated this theory, and
intracranial circulation is not dependent on the
cervical sympathetic system7
• Vascular Hypothesis7,16
• Vertebrobasilar ischemia thought to arise
secondary to arthritic spurring, upper cervical
instability (UCI), atherosclerosis, arterial
dissection, or embolism of vertebral arteries
• Collateral circulation should compensate,17-18
but perhaps not in older individuals with
atherosclerotic disease19,and anatomic
variation is common17,20
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Proposed Mechanistic Theories
• Vascular Hypothesis - continued
• However, vertebrobasilar ischemia often
accompanied by additional signs & symptoms:
TIAs, visual disturbance, weakness, perioral
paresthesia, syncope, tinnitus, etc.20-21
• The possibility of Cervical Arterial Dysfunction
(CAD) should be considered.
• No definitive differential test, but consider
presenting signs/symptoms and historical risk
factors in clinical reasoning
CAD Signs and Symptoms22-24
ICA
Non-Ischemic
Sy/Sx
• Head/Neck Pain (often
around TMJ & temporal
region)
• Horner’s Syndrome
• Tinnitus
• CN Palsies (often IX-XII)
Less Common:
• Ipsilateral carotid bruit
• Scalp Tenderness
• Neck Swelling
• CN VI (Abducens) palsy
• Orbital Pain
• Anhidrosis
ICA Ischemic
Sy/Sx
• TIA
• Ischemic
Stroke
• Retinal
Infarction
• Transient
Visual
Disturbance
VBC
Non-Ischemic
Sy/Sx
• Ipsilateral
Neck Pain
“unlike any
other”
• Occipital
Headache
• C5/C6 NR
Impairment
(rare)
VBC
Ischemic
Sy/Sx
• “5 D’s and 3 N’s”
• Ataxia
• Hoarseness
• Clumsiness
• Agitation
• Photophobia
• Limb Weakness
• Anhidrosis
• Hearing disturbance
• General malaise
• Short-term memory
loss
• Various CN palsies
*Key: ICA: Internal Carotid Artery, VBC: Vertebro-Basilar Complex
CAD Risk Factors24
Proposed Mechanistic Theories
• Hx of Trauma
(*even “trivial”)
• Hx of Migraines
• Hypertension
• Hyperlipidemia
• Cardiac Disease
• Vascular Disease
• Previous CVA or TIA
• Diabetes
• Altered Somatosensory Input Hypothesis7,16
• Clotting Disorders
• Anticoagulant Therapy
• Long-term Steroid Use
• Hx of Smoking
• Recent Infection
• Immediately PostPartum
• Absence of plausible
mechanical explanation
• Prevailing theory to explain CGD
• In review, cervical somatosensory input is
processed along with vestibular & visual input for
postural stability & awareness of the body’s
position in space.
• Remember also the specific involvement in the
cervicocollic, cervicoocular, and tonic neck
reflexes
Proposed Mechanistic Theories
Disturbed Head-Neck Awareness
• Altered Somatosensory Input Hypothesis – cont.
• Often objectively measured via relocation tests and
describe Joint Position Error (JPE)
• Cervical dysfunction results in altered
somatosensory input from the upper cervical
spine5,7,13 which may in turn result in a sensory
mismatch with the vestibular and visual input,
and/or result in disturbances in head-neck
awareness, neck motor control, postural stability,
or oculomotor control5.
• Several studies have noted impairment in those with
both traumatic and atraumatic neck pain25-28
• Patients may complain of feeling their head is
wobbly5 or may demonstrate poor awareness of
neutral head posture
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Disturbed Neck Motor Control
Disturbed Postural Stability
• Patients with neck pain may have inadequate support
from the deep spinal stabilizers29-30
• Increased activation of superficial musculature is
thought to compensate5
• This may overload already painful structures and
impact kinesthetic sense and control, which in turn
may cause uncertainty and further guarding5
• Patients may present with complaints of jerky neck
movements, fatigue, or a “heavy head” 5
• Altered afferent input from the upper cx spine may
create a “sensory mismatch”
• Multiple studies have demonstrated disturbed
postural stability in those with neck pain31-35
• Dizziness may be described as unsteadiness,
insecurity, light-headedness, or tipsiness
• Typically vague, and without true vertigo
• Symptoms associated with neck movement, or with
times of day with increased stiffness or fatigue
Disturbed Oculomotor Control
Other Studies of Interest
• Deficits in smooth pursuit, saccadic eye
movement, and gaze stabilization have been
noted in patients with neck pain in multiple
studies5,26,36-40
• One study40 correlated oculomotor dysfunction
to increased postural sway in WAD
• Patients may complain of mild visual disturbance
or problems with reading
• Deficits of smooth pursuit, gaze stability, and/or
saccadic eye movements may be noted
• Karnath and colleagues noted impaired subjective
interpretation of the “straight ahead” position during
and after vibration of the posterior neck
musculature, but this appeared to be compensated
when visual input was allowed 41
• Lennserstrand et al demonstrated visual movement
illusion and actual eye movement on vibration
stimulation of neck muscles42
• Bove and colleagues noted deviations during
walking43 and stepping in place44 when vibratory
stimulation was applied to neck musculature either
before or during the desired action
Other Studies of Interest
• Duclos et al found impaired postural sway for
up to 14 minutes after a 30s voluntary
contraction of various neck muscles45
• Gosselin et al noted impaired balance via
posturography after cx extensor fatigue46
• Schmid and colleagues found that neck
extensor mm. fatigue resulted in posterior
displacement when subjects were asked to
step in place47
Cervicogenic Dizziness:
Manual Therapy Interventions
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Lystad 2011 SR48
2005
• 1 RCT (Karlberg 1996) used joint mobilizations as part of
comprehensive treatment vs no treatment
• Only 17 patients
• No blinding
• 9 non-RCTs
• 4 used cervical manipulation
• General poor quality
• “moderate evidence to support the use of manual
therapy, in particular spinal mobilisationand
manipulation, for cervicogenic dizziness.
• The evidence for combining manual therapy and
vestibular rehabilitation in the management of
cervicogenic dizziness is lacking”
Conclusion: Level 3 evidence for manual
therapy treatment of CGD12
Manual therapy combined with
vestibular49
2006
• Schenk 2006
• “Cervicogenic Dizziness: A Case Report Illustrating
Orthopaedic Manual and Vestibular Physical
Therapy Co-management”
• 41 patients (treatment vs. control)50
• High-velocity and low-amplitude manipulation, proprioceptive neuromuscular
facilitation, ischemic compression of myofascial trigger points, and spinal
rehabilitation exercises aiming to normalize cervical range of motion (CROM)
and head relocation accuracy (HRA)
• Excluded neck trauma
• No mention of blinding
• VAS decrease 29 mm
• Sig change in HRA
• No change ROM
Outcomes
2014
+ self-SNAG
Up to 3 hypomobile or painful joints
+ ROM exercises
Detuned laser
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2008
• 34 participants
• 4-6 treatments of SNAGS or detuned laser
• “Double-blinded”
{{PIC OF SNAG}}
Yang 201553
• “Conducting both cervical stability training and
upper thoracic manipulation for patients with
chronic neck pain was more helpful for the
improvement of proprioception and pain than
cervical stability training alone.”
• Low sample size
• No effect sizes or CI reported
An uncomfortable case report…
• Positive patient outcome after manual cervical
spine management despite a positive vertebral
artery test (Johnson 2008) 54
Cervicogenic Dizziness:
Targeted Exercise Intervention
Evidence
Evidence
• Role of muscle spindle afferents in the feedback
mechanism
• Suggests that management addresses the local causes of
abnormal cervical afferent input
• Links between systems and secondary adaptive changes in
the sensorimotor control need to be considered
• Plasticity in the CNS
• Goal of intervention is to modulate the mismatch of afferent
input from the proprioceptive, visual and or vestibular
systems to the sensorimotor control system
• Over-stimulation
• Under-stimulation
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Clinical Reasoning
Clinical Reasoning
• Muscle imbalance
• Hypersensitivity- pain response, SNS
• Increased fatiguability
• Degenerative changes such as fiber transformation, fatty
infiltration and atrophy of the neck muscles
• Altered mm spindle sensitivity affecting cervical afferent
input
• Joint mobility impairment
• Compromised joint stability
• Exercise can reduce sensitivity (walking and neck pain)
• Ischemic or inflammatory events
• Reflex joint inhibition of muscle spindles
• Proprioceptive training
• Sensorimotor control deficits more pronounced in pts
with WAD and c/o dizziness, unsteadiness, or visual
disturbances
Clinical Reasoning
Clinical Management
• Disturbed Head-Neck Awareness
• Neuromuscular control training to improve
cervical position sense
• Relocation tests for natural head posture (NHP)
• Pts who overshoot targets when position sense is
measured may have disordered cervicocollic reflex
inhibition
• c/o “wobbly head”, poor positon sense
• Cervical muscle endurance training to improve
balance
Clinical Reasoning
Clinical Management
• Disturbed Neck Movement Control
• Disturbed Neck Motor Control
• Unable to reliably detect minor segmental instabilities in
the c/s, hotly debated topic regarding the definition of
hypermobility
• These minor segmental instabilities are thought to be
causative in early spinal degenerative change and has
been seen in women with chronic WAD
• Clinical presentation: jerky neck mvmt, intense fatigue,
heavy head
• Treatment:
• Muscular control, i.e. DNF
• Timing
• Decrease compensatory activation of superficial cervical
musculature
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Clinical Reasoning
Clinical Management5
• Disturbed Postural Stability: Dizziness and/or Unsteadiness
• Concerned with sensorimotor disturbances from the cervical spine
structures
• Altered sensory input can disturb an intact vestibular subsystem=
“sensory mismatch” theory
• System can become adept at compensating though underlying
dysfunction remains, impt to screen pts with neck pain for balance
problems even though they may not complain
• Static standing balance= increased postural sway or rigidity on firm
surface with EC, 30sec, or in tandem stance
• Pt c/o “spinning in the head”, unsteadiness, lightheadedness, tipsy,
more pronounced in a.m with stiffness and in p.m. with fatigue,
quick mvmts provoke, walking in dark or watching moving objects
• Difficult to differentiate from vestibular etiology, but symptoms
usually more subtle
Clinical Reasoning
• Oculomotor Disturbances
•
•
•
•
•
•
Decreased smooth pursuit velocity gain
Altered velocity and latency of saccadic eye movements
Increased gain of the cervico-ocular reflex
Test: Smooth pursuit neck torsion test (Tjell et al 129)Pts c/o changes in visual system
Assess via examination of oculomotor control
Kristjansson E and Treleaven J.
Sensorimotor function and
Dizziness in Neck Pain:
Implications for Assessment and
Management. J Orthop Sports
Phys Ther. 2009;39(5):364-377.
Oddsdottir G. Cervical Induced
Balance Disturbances After Motor
Vehicle Collisions: The Efficacy of
Two Successive Physical
Treatment Approaches [thesis].
Reykjavik, Iceland: University of
Iceland; 2006.
Clinical Management
• Eye-neck coordination
exercises standing on an
unstable surface
• Eye movement training
Clinical Reasoning
Exercise to complement manual
interventions
• Psychomotor
• How do we determine vigor?
• Over-exposure
• Graded exposure
• Evidence from neurogenic dizziness populations shows…
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Specific Exercise
• SNAGs
• AROM
• VOR?
Cawthorne-Cooksey Exercises
(with some modifications)
Seated
•
• Treatment considerations
• Effectiveness in CGD populations
• OUTCOME measures
•
Eye, head and shoulder movements
•
Eye movements -- at first slow, then quick
•
up and down
•
from side to side
•
focusing on finger moving from 3 feet (1 metre) to
1 foot (30 centimetres) away from face
•
Head movements at first slow, then quick, later
with eyes closed
•
bending forward and backward
•
turning from side to side
•
turning head up and down (as in nodding)
•
Shoulder shrugs, shoulder rolls, shoulder elevation,
combined shoulder elevation with head movement
Bending forward and picking up objects from the ground
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Standing
• Eye, head and shoulder movements as before
• Changing form sitting to standing position with eyes
open and shut
• Throwing a small ball from hand to hand (above eye
level)
• Throwing a ball from hand to hand under knee
• Changing from sitting to standing and turning around in
between
Moving about
• Circle around center person who will throw a large ball
and to whom it will be returned
• Walk across room with eyes open and then closed
• Walk up and down slope with eyes open and then
closed
• Walk up and down steps with eyes open and then
closed
• Any game involving stooping and stretching and aiming
such as bowling and basketball
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