10/10/2014 1 Client-Centered Management for Voice Disorders: Using the ALERT model Linda Rammage, PhD, RSLP, S-LP(C) Director, PVCRP BCASLPA, 2014 What is EBP? (Hjørland, 2011) all practical decisions 1) based on research studies and 2) research studies are selected and interpreted according to specific norms characteristic for EBP norms typically disregard theoretical and qualitative studies and consider quantitative studies according to a narrow set of criteria for evidence (Random Control Trials - RCT) Tx based on other research designs considered “research-based-practice” EBP/RCT – “Gold Standard?” (Montgomery & Turkstra, 2003) Means to support clinical reasoning, not “End” Limitations in clinical research/Tx decisions: Statistical signif ≠ clinically meaningful… achieving both is a social judgement Judgement always required for indiv. client (“n of one”)… even RCT results cannot be assumed to generalize to each individual RCTs may be impractical/impossible (eg. statistical power/study N required) or design inappropriate for many clinical Q’s Cochrane Reviews (RCT): “Voice/Voice Therapy” Q: Is there evidence that any form of SLT is more efficacious for IPD? (2012) Author Conclusion: “Insufficient evidence due to small N’s” Q: Is there evidence that either direct or indirect voice training or combined is effective to prevent voice disorders in at-risk population? (2007) Author Conclusion: “No evidence from studies that met review criteria. Need larger N and better methodology (better control criteria)”
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What is EBP? for Voice Disorders: Using the ALERT model · Central Sensitization Amygdala: both enhances & inhibits pain processing Neugebauer et al. Amygdala & Persistent Pain. Neuroscientist.
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Neural plastic response to repetitive nocistimulation
depolarization
ILS: A Central Sensitivity Syndrome? (Morrison & Rammage, 2010)
Heightened sensitivity of central neurons
Altered activation thresholds, and enhanced responsiveness to synaptic inputs as with neuropathic pain (Woolf CJ, Slater MW. Science 2000; 288:1765-8)
Underlying Neuro-Endocrine-Immune (NEI) pathology? (Morrison et al, 1999; Yunus, 2000-2008)
CS verified by testing neurotransmitters, neuro
modulators with nociceptive spinal flexion reflex, Functional MRI and cerebral evoked potential by ElectroEncephaloGraphy (Yunus, 2005; 2007)
Central Sensitization
A defined input, or sensory stimulus, produces a sensory experience greater in amplitude and duration than would be expected
The sensitivity of the pain system is shifted such that normally innocuous inputs can activate it & perceptual responses to noxious inputs are exaggerated, prolonged & widely spread
This could represent a central amplification due to increased excitation or reduced inhibition
Normal Sensation
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Central Sensitization Amygdala: both enhances &
inhibits pain processing
Neugebauer et al. Amygdala & Persistent Pain. Neuroscientist. 2004 10:
Orbitofrontal cortex not functional at birth. Over the
1st year, limbic circuitries emerge in sequence:
amygdala ant cingulate insula orbitofrontal
The Attachment System
Attachment system improves chances of infant’s
survival
seeking proximity: protection from harm, attack,
separation from group
Attachment relationships crucial in organizing
neuronal growth of developing brain
emotional relationships have direct affect on
development on memory, narrative, emotion
regulation
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Genetic factors vulnerability for a disorder,
environmental factors, such as attachment, play
crucial role in ultimate expression of symptoms
In postnatal period there is genetically driven
overproduction of synapses
Pruning & maintenance of synaptic connections
in frontal, limbic, & temporal cortices influenced
by psychological factors
Early abuse experiences of neglect/trauma
excessive pruning = poor limbic connections …
Human connections create neuronal connections:
Major environmental factor in brain development
Affect regulation pathway:
orbitofrontal limbic system
Orbitofrontal
Cortex
Attachment experience
development of orbitofrontal
function affect/behavior
regulation
Orbitofrontal metabolic
dysfunction in autism,
schizophrenia, bipolar,
depression, PTSD, drug
addiction, cluster B
personality disorders
Attachment pattern
Child Caregiver
Secure Uses caregiver as a secure base for exploration. Protests caregiver's departure and seeks proximity and is comforted on return, returning to exploration. May be comforted by the stranger but shows clear preference for the caregiver.
Responds appropriately, promptly and consistently to needs. Caregiver has successfully formed a secure parental attachment bond to the child.
Anxious Clingy, unable to cope with absences of the caregiver. Seeks constant reassurances.
Excessively protective of the child, and unable to allow risk-taking, and steps towards independence.
Avoidant Little affective sharing in play. Little or no distress on departure, little or no visible response to return, ignoring or turning away with no effort to maintain contact if picked up. Treats the stranger similarly to the caregiver. The child feels that there is no attachment; the child is "rebellious" and has a lower self-image and self-esteem.
Little or no response to distressed child. Discourages crying and encourages independence.
Child and caregiver behaviour patterns before the age of 18 months
[Ainsworth et al, 1978; Main & Solomon, 1986]
Ambivalent/
Resistant
Unable to use caregiver as a secure
base, seeking proximity before
separation occurs. Distressed on
separation with ambivalence, anger,
reluctance to warm to caregiver and
return to play on return. Preoccupied
with caregiver's availability, seeking
contact but resisting angrily when it
is achieved. Not easily calmed by
stranger. In this relationship, the
child always feels anxious because
the caregiver's availability is never
consistent.
Inconsistent between appropriate
and neglectful responses.
Generally will only respond after
increased attachment
behavior from the infant.
Disorganized Stereotypies on return such as
freezing or rocking. Lack of coherent
attachment strategy shown by
contradictory, disoriented behaviours
such as approaching but with the
back turned.
Frightened or frightening
behaviour, intrusiveness,
withdrawal, negativity, role
confusion, affective
communication errors and
maltreatment. Very often
associated with many forms of
abuse towards the child.
Attachment
pattern Child Caregiver
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Avoidant attachment history biased toward
parasympathetic state: low arousal, reduced
emotionality; under stress vulnerable to
overregulation & internalization
psychopathologies
Ambivalent attachment sympathetic state:
high arousal, high emotionality; under stress
vulnerable to externalizing psychopathologies
Attachment and Psychopathologies (Main et al, 1987)
Common forms of psychopathologies Numerical values are path coefficients, representing the strength of
associations between constructs (Krueger & Markon, 2006)
Levels of Emotional Awareness (Lane & Schwartz, 1987; Lane, 2008)
• Cognitive developmental process
• Similar to Piagetian theory
• 5 basic levels follow developmental pattern:
infants to “fully aware” humans
• neurobiological correlates
• top-down modulation allows “aware” person to
regulate amygdala and change physiological R’s
(eg. relaxed breathing to stop fight-flight R’s) Parallels in the hierarchical organization of emotional experience,
and neural substrates. Levels filled in white are implicit levels;
those in grey are explicit levels. Lane & Schwartz, 1987
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LEVEL 5: PREFRONTAL
CORTEX ; ant cingulate,
medial prefrontal cortex
Reflective awareness:
complex analysis of
experiences of self and others
LEVEL 4: Blends of emotions: “I feel
disappointed with myself”
LEVEL 3: ant cingulate, insula,
temporal lobe, orbitofrontal
cortex
Single emotions: “I feel
sad/happy/angry”
LEVEL 2: amygdala, thalamus,
basal ganglia
Sensorimotor enactive; crude
distinctions between globally
+ or – states; gestures &
mvts: “I want to hit you!”
LEVEL 1: thalamus,
hypothalamus, brainstem
Automatic generation of
emotional responses: “My
stomach/throat/jaw hurts”
Neuroanatomical Model: Implicit VS
Explicit Emotional Processes (Lane, 2000)
Amygdala and Thalamo-Amygdala process
implicated in rapid, low-level implicit (sub-
conscious) processing of stimuli. Precedes
emergence of emotional “feeling” state.
Phylogenetically-older structures, protect
organism in life-threatening situations.
In contrast, Neocortical-Amygdala pathway
involved in slower, more differentiated
explicit (conscious) processing of stimuli.
Implicit and Explicit Processes (Post Piagetian Representational Redescription)
Implicit (automatic action/sensori-motor)
patterns of knowledge (Levels 1 & 2) are
transformed to Explicit (conscious: Levels 3-5)
representations through language.
(Karniloff-Smith, 1992)
Use of language to describe emotions modifies
one’s emotional awareness and experience at
conscious levels. (Werner & Kaplan, 1963)
Corresponds with “Top-Down” modulation of
emotional responses.
Implicit Processes
May induce postures in respiratory and laryngeal mechanisms to facilitate rapid/strong physical reactions, as in fight or flight: fixing thorax with vf adducted to enhance upper body strength / abducting vf to facilitate free respiration for running.
Absence of higher level emotional processing and lx/respiratory system postures not conducive to normal phonation may make individual more susceptible to muscle tension voice/laryngeal disorders.
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Baker & Lane, 2009
Implicit emotional responses reflect
“unformulated experience”: emotions not fully
formed/differentiated, so expressed 10
physically. Once discussed & processed, can
be experienced fully.
VS: Freudian concepts: unconscious fully
formulated emotions being repressed
Theory informs treatment approach
Explicit Emotional
Experience
Anatomical
Correlates:
1- ventro-medial
prefrontal cortex;
right parietal
cortex; insula,
temporal pole
2 - dorsal ACG
3 - paracingulate
region of medial
prefrontal cortex
Explicit Emotional Processes support cognitive neuroscience approach to emotion.
Engage paralimbic and neocortical
structures that are not specific to emotional processes.
Domain-general nature of these structures infers they compete with other (potentially interfering) input for conscious processing.
May explain differences in individual attention to and use of emotional info.
Explicit processing may make individuals less vulnerable to physiological states associated with muscle tension dysphonias.
Top Down Modulation
Bodily sensations
Action tendencies
Discrete Emotion
Blends of Emotion
Self reflection
Brainstem
Diencephalon
Limbic
Paralimbic
Prefrontal Cortex
PSYCHOLOGICAL NEUROANATOMICAL
Greater activity in
dorso-medial
prefrontal cortex
associated with
higher vagal tone (thus, reduced HR,
calming)
Verbal emotion
labelling inhibits
amygdala activity. (Amygdala preferentially
activated by aversive
stimuli.)
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The LEAS - Levels of Emotional
Awareness Scale (Lane et al, 1990)
Written performance measure
Patients describe anticipated reactions for
self and other person to short vignettes
Scored per specific structural criteria to
determine degree of specificity of emotion
words and range of emotions
Scoring unbiased by patient or rater due to
structure focus of criteria
Glossary for each level guides scoring
Examples of LEAS 0-5 scoring – “Self” and “Other” R’s given separate scores
Non-affective (non-emotional) words = 0
Physiological words to describe feelings = 1
Undifferentiated emotion (eg. I’d feel bad) or
action tendency = 2
Single word used conveying differentiated
emotion (eg. I’d feel happy/sad/angry) = 3
Two or more level 3 words used to enhanced
differentiation = 4
“Self” and “Other” scores = 4 and
differentiated = 5
LEAS Reliability & Validity
High inter-rater reliability; high internal
consistency (Lane et al, 1998)
Construct validity supports LEAS as measure
of cognitive-developmental continuum:
moderately positive correlations with other
cognitive-developmental measures: Sentence
Completion Test of Ego Dvlpt and Cognitive
Complexity of the Description of Parents (Lane, 2008)
Emotion Processing Deficits and
Psychosomatic Voice Dysfunction
Causal Model of Emotion Processing Deficits in
Women with “FVD”: more severe events/
difficulties, COSO events/difficulties, highly
anxious coping style, less emotionally
expressive families, more ambivalence re
expressing neg. emotions.
FVD result of strong negative emotional
reactions to events + emotional processing
interference.
(Baker et al, 2007; Baker, 2008)
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Childhood Abuse in Patients with
Conversion Disorder (Roelofs et al, 2002)
Compared patients with conversion to
patients with affective disorder with respect
to childhood abuse
Patients with conversion reported higher
incidence of physical/sexual abuse
Larger number of different types of abuse,
longer lasting incidents of sexual abuse,
more incestuous experiences
What to screen for in initial
assessment: Attachment experience:
History of trauma or abuse
Quality of relationships (family, partner, school, friends)
Significant acute stressor in an otherwise well functioning individual
Depression, anxiety
Observe: Postural/Gestural/Facial Postures
Voice / posture changes with topics
Lexicon used to describe significant
events/distress
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Anatomical
Factors:Aging, Lesion
Disease
Lifestyle:Acoustics
Environment
Ergonomics
General health
Occupational demands
Vocal dose
Emotion:Anxiety
Depression
Symbolic conversions
Vocal expression
Vocal repression
Level of emotional
awareness
Reflux:Diet
Eating habits
Genetics
Medications
Posture
Weight
Technique:Alignment/Posture
Muscle misuses:
Neck/Shoulders
Face/Jaw/Tongue
Pitch focus
Resonance focus
Speech breathing
Reflux
71% MTD Patients =/> 4/7 Reflux Sx, Vs
VC Population: 47% (2009, N=472)
Higher palpation scores for Thyro-hyoid *
and Pharyngeal Constrictors
Higher % with A-P compression *
Reflux increases Lx tension and exacerbates
co-existent dysphonia (Gill & Morrison, 1997)
Reflux control facilitates therapy and recovery
Reflux Factors
Reflux - LPR
Common Symptoms:
throat sensations, am dysphonia
waking at night coughing or choking
habitual throat clearing; chronic cough
globus pharyngeus
heartburn
“post-nasal drip”
adductory laryngospasm
asthma or other chronic breathing difficulties
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Common Signs:
erythema / edema: posterior glottis
sub-glottis
arytenoids
contact ulcer / granuloma
“pseudo-sulcus”
Contact Granuloma
“… but Doctor, I don’t have
heartburn!” 2011 (www.pvcrp.com)
Patient tutorial on LPR
Diagrams, script and vocal narration
Patient compliance self-ratings (Likert scale)
(Targeted) Lifestyle changes compliance (LC)
Medication compliance (MC)
Tutorial group (N= 20) LC: 19/20 high compliance
MC: 16/20 high compliance
No tutorial group (N=20) LC: 9/20 high compliance
MC: 14/20 high compliance
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Anatomical
Factors:Aging, Lesion
Disease
Lifestyle:Acoustics
Environment
Ergonomics
General health
Occupational demands
Vocal dose
Emotion:Anxiety
Depression
Symbolic conversions
Vocal expression
Vocal repression
Level of emotional
awareness
Reflux:Diet
Eating habits
Genetics
Medications
Posture
Weight
Technique:Alignment/Posture
Muscle misuses:
Neck/Shoulders
Face/Jaw/Tongue
Pitch focus
Resonance focus
Speech breathing
Technique
Bad habits become programmed by repetition
(Neural Plasticity / Motor Learning)
Postural misuses:
• neck, back, head/shoulders?
• Speech breathing patterns ?
• Lower face, jaw and tongue?
• Infra-hyoid muscles?
• Specific Misuse Patterns – Larynx/Glottis
Technique
Posture affects breathing
Look at :
Back Alignment (Lordosis; Scoliosis)
Shoulders/Scapulae
Head-Neck Relationship
Stance
Knees
Use of Furniture; Props
Mal-Adaptive Speech Breathing
Behaviours affect Glottal Closure
abs clenched: thoracic elevation
large lung volume: laryngeal pull,
results in greater glottal chink plus
compensatory hypervalving (Sundberg et al,
1991; Sundberg, 1999)
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Normal inspiration and
expiration for
speech/singing, compared
with two common
misuses: failure to use
inspiratory “checking”
forces during phonation
(top right); and
exaggerated abdominal
tension to “support” the
production of voice
(bottom right). Both these
misuses can lead to
hyper-valving in the larynx
to regulate airflow.
Aligned posture and
common patterns of
misalignment
Scapula
adduction
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Head-neck relationships. Neutral is “healthy” posture. Chronic
neck extension or flexion impact the laryngeal suspension
system and can affect voice and swallowing.
Neck Tension / Headaches and MTD (Self-Reported, PVCRP, 2009; N = 472)
Tension Site 10 MTD Non- MTD
Neck /
Shoulders
46% 28%
Chr. Headache 27% 13%
Both 15% 10%
Totals 88% 51%
Palpation Sites: Anterior Floor of
mouth: Supra-hyoids:
- at rest
- pitch glides
- speech, probes
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“Scalloped” tongue periphery from pressing the tongue against the teeth.
Common in individuals who misuse muscles of the jaw and tongue:
tension in supra-hyoid muscles and jaw clenching are typically
associated with this visual perceptual sign.
Thyrohyoids: - at rest, yawn
- pitch glides
- speech, probes
Cricothyroids:
- at rest, yawn
- pitch glides
Pharyngeal Constrictors - at rest
- phonation
Jaw-Tongue Functions
Critical anatomical links to larynx
Facial co-contraction patterns common
(eg. Eyebrow adduction + jaw clench)
FACS studies: upper face emotionally
more salient, therefore Tx targets both
54% of MMD patients “TMJ” dysfunction
vs. 22% non-MMD patients (excluding
ILS) (PVCRP, 2009; N = 472)
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TMJ: - opening; closing
- speech; singing
Sub-occipitals: - at rest
- pivot; swivel Muscle Misuse Type 1: (Case 61)
The Laryngeal Isometric
• Generalized tension in all laryngeal muscles
• Often associated with an exaggerated posterior glottal chink
• Often associated with 20 mucosal lesions: bilateral nodules, chronic laryngitis, polypoid degeneration
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Muscle Misuse Type 2a (Case 63)
• Lateral compression at the glottal level • Frequently seen with generalized postural misuses and tension • May be triggered by an infection or by gastro-esophageal reflux
Muscle Misuse Type 2b (Case 64*)
• Supra-glottal lateral compression • Hyper-adduction of the false vocal folds • Often psychologically based
Clinical Example (*Case 64)
47 year old female experiencing globus and dyshonia after episode of sinusitis + cough. Normal exam except lateral supra-glottal compression. “Held” larynx. Static facies: eyes, lips, hypertonic masseters
Co-owner/manager of fast-food franchise with husband. Minimal marital relationship beyond work/children. During aphonia, husband had to assume more responsibility. Accused her of “faking”.
Voice Sx started in work environment, when confronting a defiant young employee about wearing perfume that she thought triggered Sx. Sx gradually generalized to many situations, including home.
Scored 5/7 on reflux Sx score (LPR; no heartburn)
Background
Alcoholic chain-smoking father, abandoned family when Pt. was 13 yoa.
Pt., eldest of several sibs, had to assume child-care responsibilities. Mother took 2 jobs, and rarely home.
A younger sister had defied Pt.’s authority and frequently caused trouble in community. Sisters fought physically over these incidents. Pt. periodically recalled those incidents when dealing with defiant employee.
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Emotional Awareness
Pt. aware of co-occurrence of exposure to noxious odors and throat Sx. (Level 1)
Also aware of desire to hit employee when she wore perfume and husband when he accused her of “faking voice loss”. (Level 2)
Preoccupation with globus led her to worry she had lx CA, to which an uncle had recently succumbed. (GP had suggested LPR, but Pt. rejected Dx). (Level 4?)
Psychological factors….
Patient abandoned by father & in a sense, also by mother (insecure attachment history = compromised emotion regulation pathway); likely had to forgo her own needs & prioritize taking care of others (siblings), little space for her to express her emotions (anger, resentment)
Development of avoidant/introversion traits that predispose to development of psychosomatic voice dysfunction
Sensory-Emotional Trigger
Interaction with defiant employee acted as a
trigger: feelings of helplessness, anger that
she felt both in the past, dealing with her sister
& in the present, dealing with the
employee/husband; in both past & present her
experience may be that her needs are not
being acknowledged/addressed
Reflux/Globus sensation increased when
emotionally aroused, due to tension in
abs/ANS… enhancing anxiety about CA
A
L E
R T
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Management Approach
Psychotherapy:
Develop therapeutic alliance: trusting, secure
attachment with therapist
Give her tools to tolerate emotional distress:
breathing exercises, relaxation strategies,
mindfulness exercises
Target expression of emotion, validate her
experiences/needs
Voice Therapy
Explanation of relationship of LPR to lx hypertonicity/globus. (“But Doctor, ” www.pvcrp.com)
Top-down facial exercises to increase awareness of & reduce static facial postures. (Rammage, 1996; 2011)
Explanation & demo of inappropriate VS appropriate larynx / vf posture for phonation.
ID and application of most accessible & salient facilitation technique to restore normal phonation (glottal fry, gradually increasing intensity, while monitoring tactile feedback with fingers over lx)
Negative practice to increase voluntary control: desensitize to triggers; create “dysphonia”; apply facilitation technique to restore normal phonation.