Objective Measures of Voice and ISBAR Flashcards
What is the cut-off for ‘normal’ voice for HNR?
What is the cut-off for perceptual clarity?
20+
25+
What ‘mini-baseline’ tasks should we collect during every therapy session (and record!)
- Have a conversation (not performative - good for typical quality comparison)
- The Rainbow Passage (Fairbanks, 1960) - same words each time - look at particularly dysphonic phrases
- CAPE-V phrases
- Prolonged vowel ‘ah’ ~5sec (for HNR)
In PRAAT, which part of the sample do we analyse for HNR?
The ‘best’ bit of the MPT (when the voice is most stable & there is less ‘noise) –> if pitch isn’t stable or there is too much noise, MPT reading will be inaccurate (PRAAT can’ t analyse the data).
Mean of SD of F0 in women for prolonged vowel.
SD 1-3
*If type II voice or above note this + that results should be interpreted with caution.
Mean F0 for reading The Rainbow Passage (women aged 40-49)
- 8Hz
* culture may impact
(Baken + Orlikoff, 2000)
Conversational mean for women (40-49)
170.5Hz
Berg et al., 2016
Perceptual ‘hoarseness’ or roughness of a voice correlates to lower WHAT scores in PRAAT?
HRN (Harmonic-to-noise ratio)
also to higher shimmer and jitter
Functional tasks are part of which subjective assessment?
Vocal Function Assessment
Types of voices (for acoustic analysis)
Type 1 - Periodic
Type 2 - Some bifurcations/subharmonics
Type 3 - Chaotic, aperiodic
Type 4 - stochastic noise (oesophageal voice, post laryngectomy)
Harmonics are multiples of F0. F0 is the rate of vibration of the vocal folds. In a good, clear voice there will be more energy (darker bands) in which harmonics?
The lower ones
Which voice types can you take and objective measure of pitch (F0) from?
Types 1 and 2
What is jitter?
very small purturbations of the rate of vocal fold vibration (tiny fluctuations in the superior lamina propria that aren’t quite in the rhythm of the vibration)
What is shimmer?
Irregularity in the amplitude (degree of opening of the vocal fold due to small changes in subglottic air pressure/irregularity on vocal fold etc)
Can jitter and shimmer be analysed in a clinically relevant way?
No - values change according to volume, background noise, position of microphone…
The standard deviation of pitch on an F0 measure during MPT/prolonged vowel tells us what?
How well the patient can keep their pitch stable.
1-3 is normal SD
Which functional task to we use to analyse Mean F0?
Connected speech –> The Rainbow Passage (because there are norms reported) BUT F0 during reading is higher than just conversational speech.
Which functional task to we use to analyse Max / Min F0?
Pitch range task (ie pitch glides)
Which functional task to we use to analyse F0 SD?
Prolonged vowel
Which functional task to we use to type the signal (voice type 1, II, II or IV)?
Prologed vowel
Which functional task to we use to analyse HNR, Shimmer, Jitter?
Prolonged vowel
Which functional task to we use to analyse CPP (Cepstral Peak Prominence), LTAS (Long-Term Average Spectrogram)?
Connected speech (n/s if The Rainbow Passage or conversation?)
Which functional task to we use to analyse mean amplitude?
Connected speech (n/s if The Rainbow Passage or conversation?)
Which functional task to we use to analyse Max/Min amplitude?
Dynamic Range task (loudness task)
–> usually as people become less dysphonic, the difference between their quietest and loudest sounds increase.
What does an electroglottograph measure?
take a simultaneous audio-recording
True Vocal folds being in contact (circuit completes when true vocal folds come into contact - voltage increases)
MODAL - LONGER PERIOD OF OPEN/CLOSE AND FEWER CYCLES PER SECOND.
FALSETTO - SHORT PERIOD OF TIME WHEN VOCAL FOLDS ARE TOUCHING COMPLETELY - VOCAL FOLDS OPEN FOR LONGER.
PULSE (fry) - DOUBLE PEAK CORRESPONDS TO PERIOD OF CLOSURE. UNIQUE PATTERN.
Electroglottography
ORAL PRESSURE IS EQUIVALENT TO SUBGLOTTIC PRESSURE (EXCEPT AT VERY HIGH/LOW PRESSURE) THE AMOUNT OF PRESSURE REQUIRED TO BEGIN VOCAL FOLD VIBRATION.
- so how to test subglottic pressure?
/p/ /p/ /p/
(sound released on full lip-closure, prior to vowel)
Measures larnygeal resistence (measure of closure) - can help with diagnosis
Inducible laryngeal obstruction (ILO) [narrowing of larynx in response to triggers like exercise]. Measured by ENT how?
Air Volume Measures ie Wet Spriometer and lung volume (measures of movement of abdomen and rib cage movement during breathing - Plethysmograph. Calibrated with spirometer and airflow)
What are physiological Assessments that measure electrical signal (action potential) in muscles used for?
(done by ENT or neurologist)
Electromyography
- locate specific muscles (ie for botox injection to treat spasmodic dysphonia)
- Diagnoses muscle paresis or paralysis
2 types of electromyography:
–> auditory signal for muscle activation
- Surface (non-invasive, but only surface muscles can be measured)
- Fine Needles (invasive, but can measure deeper muscles)
How many people with MTD have secondary pathology?
20% no secondary pathology
(80% do have secondary pathology!)
MTD can also occur as a reaction [compensation] to preexisting organic conditions ie URTI, nodules etc due to phonotrauma, VF paresis, nodules etc)
6 disorders that can arise secondary to vocal fold trauma:
- Inflamation, chronic laryngitis
- Oedema, Reinke’s oedema
- Vocal nodules
- Contact ulcers
- Polyps
- Sulcus vocalis
Hourglass closure pattern…
Vocal nodules
OVD Type 1 - Benign mass lesions or tissue changes
Common benign tumour in adults/children. Whitish cluster of tissue (rasberry texture), Can proliferate and obstruct the airway
Papilloma
OVD Type 1 - Benign mass lesions or tissue changes (Baker, 2007)
Most commonly a complication of intubation, can be related to GERD, Usually affect the vocal processes of the arytenoids
Laryngeal granulomas
can interfere with VF closure - affect voice
OVD Type 1 - Benign mass lesions or tissue changes (Baker, 2007)
Increase VF mass and stiffness, impacting voice quality. 1. Flat white, plaque like lesions 2. warty lesions. Can be premalignant - should be closely monitored
- Leukoplakia
2. papillary keratosis
Only 2 organic voice disorders (Baker’s 2007 classification) where therapy can change the voice with good efficacy
- Vocal fold paresis
2. Parkinson’s disease (Lee Silverman)
OVD Type 1 - Benign mass lesions or tissue changes (Baker, 2007)
Whitish mass of tissue in the interarytenoid space. Relatively rare, unknown aetiology.
Pachydermia laryngis
OVD Type 1 - Malignant changes (Baker, 2007)
Cancer
OVD Type 1 - Tissue changes (Baker, 2007)
Causes include arthritis, trauma or joint disease. Difficult to distinguish from paralysis of VF. Usually requires surgical treatment.
Ankylosis of the cricoarytenoid Joint
OVD Type 1 - Tissue changes (Baker, 2007)
Often congenital, Sheet of tissue between VF, usually anterior end. Paediatric symptoms: weak cry, difficulty breathing and stridor. If extensive in a baby, may require tracheotomy
Laryngeal web
**If the male voice doesn’t get deeper at puberty, this may be a cause. Causes limited pitch range.
OVD Type 1 - Vascular disorders (Baker, 2007)
Rupture of blood vessels -> bleeding into submucosal layer. Cause may be single episode of traumatic voice use or trauma. Usually unilateral, can be bilateral. More common in women.
Haemorrhage
- More likley premenstrually, as VF are slightly swollen then.
- Ibuprofen/asprin/blood thinners = more likely
OVD Type 1 - Vascular disorders (Baker, 2007)
Prominent, distended, lengthened and tortuous blood vessel on the surfact of the vocal fold (varicose vein-like). May increase thickness and mass of the VF. May be a ‘herald vessel’ –> sign that there is bleeding into the vocal fold, which will increase thickness and mass.
Varix / Ectasia
OVD Type 2 - Laryngeal Trauma (Baker, 2007)
Perceptually severely hoarse
List 3
- Aphonia/dysphonia due to blunt/penetrating injuries
- Compound fracture to thyroid cartilage
- Subluxation (partial dislocation) of arytenoid
OVD Type 4 - Neurological (Baker, 2007)
Rare. Develops spontaneously in midlife (may be genetic). Can be triggered by sever illness or psychological trauma. Improves with alcohol consumption. Cortical (UMN) disorder. Singing, reading poetry etc can reduced sypmptoms during activity.
Adductor / Abductor spasmodic dysphonia
OVD Type 3 - Neurological Lower Motor Neuron (LMN) (Baker, 2007)
Aphonia/dyphonia due to vocal fold paralysis/paresis. Can affect swallowing due to lack of laryngeal closure.
Some causes?
Damage/injury to RLN/SLN
- Nerve damage after viral infection.
- Thyroid surgery
- Tumours
- Trauma
- Radiation
- Brainstems stroke
Inducible laryngeal obstruction (ILO) / Paradoxical vocal fold movement/disorder (PVFM/PVFD)
-Vocal fold closure throughout respiratory cycle, including inspiration
-Often mistaken for asthma but difficulty is inhalation (stridor)
**Strong association with chronic cough.
WHAT ARE THE 2 TYPES?
Exercise induced: higher incidence in young, female athletes
Smell induced: Often triggered by uncontrolled reflux, perfumes, seasonal plants etc
Chronic cough/throat clearing - laryngeal hypersensitivity
-What can an SLP do?
- Make sure they’ve been referred to a respiratory physician for assessment.
- work on cortical control of cough (it is a reflex activity with elements of voluntary control)
MTD Type 1 - No secondary pathology (Baker, 2007)
- Dysphonia with palpable tension in extrinsic and intrinsic musculature.
- perceptually breathy/strained/rough
- CAN be improved (should resove) through voice therapy techniques –> should be observable in Therapy Trial (part of assessment)
PVD Type 1 - Aphonia
PVD Type 2 - Dysphonia
Loss of volitional control of the onset and sustained normal phonation. Absence of any structural or neurological pathology. Normal voice often heard in unconscious moments or during reflex activities (laugh, cough). Psycho-social factors frequently linked with onset.. but not always. What else may be linked with onset?
URTI - upper respiratory tract infection
(is it psychogenic, or a disturbance in the feedback system in brain…?
PVD Type 4 - Puberphonia (Baker, 2007)
- Persistence of high-pitched voice after voice change should have occured - no hormonal problems.
- Can occur in women (child-like voice) but not judged as inapproprate as in a man.
When do we do a ‘clinical handover’?
Assessment is complete
- report back to referring clinincian
- Pass the client on to someone more appropriate, to treat.
- Ask another health professional to take on a part of the clinical managment of the patient.
What is ‘clinical handover’?
Transfer of information, accountability and responsibility for a patient/group of patients.
- *The information should be clear, focused and relevant.
- *ISBAR
ISBAR?
Introduction Situation Background Assessment Recommendation
ISBAR
-INTRODUCTION
- Name, title, role (clinician doing handover) and LOCATION
- Patient identifiers (3 in hospital - MRN, Name, DOB) + gender
**In written report clinician details coe in letterhead or end sign-off
**Letter patient details -> Dear Dr. (name), Re: Patient name, DOB
ie Referral from Dr X.Y., ENT at RMH. Thank you for seeing Luke, a 7 year old by about his voice…
ISBAR
-SITUATION
What is going on with the patient
- *Patient came to me requiring (type) Ax. Referral from Dr Y for (Complaint/condition). Patient was looking for treatment plan….
- *Luke has been husky for about a year. His teachers have commented but his mother seems not to be too concerned.
ISBAR
-BACKGROUND
What is the clinical background/context
- Symptoms, onset, variability *Other health conditions
- ALSO occupational/social background info if relevant to current problem ie Luke is a very sociable boy. Parents work, he plays soccor 3x/week
ISBAR
-ASSESSMENT
What do I (clinican doing handover) think the problem is?
- My interpretation of Ax results, with evidence (NO diagnosis). Current condition/risks/needs
- *ie Laryngoscopic examination reveals bilatoral masses at the junction of the anterior 1/3 and posterior 2/3 of the vocal folds. These are most likely vocal nodules (ENT)…
- *Luke presents with a reduced maximum phonation time, breathy voice quality and limited pitch range, which is consistent with the diagnosis of vocal nodules…
ISBAR
-RECOMMENDATION
What do I (clinician doing handover) recommend?
- Therapy, referral to another health professional for more investigation, adjustment to working arrangements to accommodate reduced vocal load?
- -> Be CLEAR about what you are requesting (transfer/review/treatment), and the TIMEFRAME it should happen in.
- *SLP to ENT ..recommend a laryngoscopic evaluation to within the next month to assess whether the vocal nodules have resolved or not.
Writing the report:
Analysing/synthesising information - not just reporting. What is important/what is not.
*Use appropriate language + tone.
Differential diagnosis
- 5 MAJOR symptoms + signs
- Case Hx info - 1. Medical History 2. Onset 3. Variability
- Compare with Disorder Classification system - Baker, 2007
- Drill down to most COMMON/LIKELY diagnosis + 1-2 alternatives (hooves, horses)
- -> auditory-perceptual features may sound the same across different diagnosis
How could visual imaging help diagnose VF paresis
Flexible - may be able to see paralysis but not paresis.
Rigid with stroboscopy could confirm diagnosis of VF paresis because it can highlight the VFs not moving together - one being a little off.
MTD Onset may coincide with an increase in vocal load or decrease in abilities…
…we may already have a high vocal load (ie teacher) and get sick. Onset is usually gradual as effort to compensate increases…
Spasmodic dysphonia and MTD are sometimes hard to tell apart. What sets them apart?
MTD will respond to therapy. Spasmodic dysphonia won’t.
Also abductor - counting in the sixties and seventies will highlight spasming open (Voiceless sounds).
Adductor - counting in eighties and nineties (voiced sounds).
Top 5 signs/symptoms - Belinda
- strain
- persistent cough
- loses voice frequently
- loud
- hayfever/allergies
Onset:
*Gradual - over 9 months but losing voice on/off for years
Variability:
*Worse with use - better with rest.
Medical History:
*Allergies *Asthma *Reflux - post nasal drip
Social History:
*Primary school teacher *2 young kids
ENT diagnosis: *MTD *LPR
Differential Diagnosis:
Most likely ENT is right - MTD and LPR
What else could it be:
- Unilateral VF paresis + MTD to compensate
- Deep lesion, scarring, sulcis vocalis
If you do therapy a lot with Belinda, and she doesn’t improve:
ISBAR to ENT -
I (introduction) S (Situation) B (background) ASSESSMENT - initial Ax + therapy done + (lack of) response to therapy + ICF limitations improved/still current
RECOMMENDATIONS - *Laryngoscopy - pls have a look to confirm diagnosis or see if paresis…
60% of diagnoses change after a patient has had a stroboscopy. True or false?
True
Voice improves with increased pitch, onset after a cold. Could be…?
unilateral VF paresis (tensioned so vibrates better)
Nodules arise because of MTD or overuse. True or false?
True
Luke - top 5 signs/symptoms: *Roughness of voice *Breathiness *Loses his voice *yells a lot *Vocal fatigue Onset: Gradual, about 2 years ago. Variability: Worse with use, better with rest. Medical Hx: unremarkable Social Hx: Soccer player, yelling, sociable (talker) Laryngologist Dx: Nodules
Differential Diagnosis most likely: Vocal nodules + MTD
What else could it be:
Cyst/polyp and contralateral lesion + MTD
Introduction Situation Background Assessment (mine) Recommendation (mine - what I recommend, what I would life followed up or checked out, How I think they should do this ie stroboscopy)
ISBAR - to handover client to another SLP, other clinician, to hand back to referring ENT/laryngologist and have all the relevant and important information ready to go.
