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Neurological voice disorders - Coggle Diagram
Neurological voice disorders
Laryngeal nerve paralyses
Superior LN paralysis
Facts about Superior LN
Innervates cricothyroid muscle
Tenses VF to increase pitch
Contributes to VF adduction
Symptoms: vocal fatigue, hoarseness, loss of vocal range, breathiness
Mgm: wait and see, surgical fusion of thyroid, cricoid cartilages
Recurrent LN paralysis
Aetiology
Congenital in chn w spina bifida
Intrathoracic neoplasms, tumours: cancers in course of RLN
Thyroidectomy-removal of thyroid gland
Aneurysms: abnormal swelling in blood vessel
Mitral valve stenosis (left auricle enlarge, stretches RLN-alters fn)
Neck trauma-penetrating injuries
Radiation-cancer in head, neck region
Systemic disease: lupus, sarcoidosis, tuberculosis, Lyme disease, Epstein-Barr virus
Idiopathic
Facts
Left RLN lesions occurs 10x more frequently cf. right RLN
RLN innervates all intrinsic muscles of larynx except cricothyroid-superior laryngeal nerve
Lesion may be uni, bilateral- bilateral means cannot phonate
2 types: adductor, abductor (affects muscles of abduction)
Voice usually excellent immediately post-op, deteriorates a little as oedema subsides, impv in one week, permanent level 2 weeks
Types
Unilateral adductor:
VF on one side will not move to midline
Bilateral adductor:
Both VFs cannot move to midline- phonation impossible
Unilateral abductor
: VF remains in fixed adducted position-affect air entry
Bilateral abductor:
both VF remain in adducted phonation-X open to allow air into lungs, respiratory difficulty
Perceptual, physiological signs
Highly variable presentation bcos of
Location of paralysed fold relative to non-paralysed fold
Whether person can compensate for the paralysis
Unilateral RLN
AB: phonation capability still preserved. Dysphonia may be present. Change to vocal quality
AD: Excessively breathy or weak voice bcos cannot bring VF tgt, increased airflow, decreased subglottal pressure
Bilateral RLN
AB: Inhalatory stridor (gasping sound), voice quite good bcos both VF weakly adducted. In some cases, pt's airway can be completely obstructed, surgical airway is required (tracheostomy below level of VF)
AD: aphonia or dysphonia depending on fixed location of VF
Mgm plan
Wait and see approach but depends on aetiology also. Wait 6-9m to allow for fnal recovery which may occur as result of nerve regeneration
Behavioural voice Tx: Voice Tx 2-6 weeks post diagnosis can significantly improve phonatory stability w/o surgery, can also be used on top of surgical intervention (eg. in bilateral paralysis)
Vocal function exercises, resonant voice Tx
1) Surgical intervention for
unilateral paralyis
: Injection of material into paralysed VF: Materials like fat, collagen, Teflon, hydroxyapatite used to plump up paralysed VF, better chance of touching free VF ; Injection into/lateral to thyroarytenoid msucle, lamina propria, usually done under endoscopic guidance
2) Implantation: insert hard material, medial to thyroid cartilage at level of VF-Type 1 thyroplasty, serves as wedge to move paralysed VF to midline
3) Arytenoid adduction: rotation of arytenoid cartilages so that tip of vocal process moves to midline
Surgical intervention for
bilateral paralysis
: tracheostomy, arytenoidectomy (removal of arytenoids) or fixing. Cordectomy (removal of all or part of VF) or cordopexy (VF lateralisation surgery)
Spasmodic dysphonia
Aetiology
Psychologically based-conversion rxn, musculoskeleton tension
Neurologically based (Most evidence for this)- organic/essential tremor, dystonia
Idiopathic-unknown origin
Onset-4th to 5th decade of life
More common in women
Often associated w URTI, emotional stress, can be gradual
Types
Adductor
Approx 80% of all cases
Phonation- true and false VF hyperadduct-too hard, too fast, in intermittent, irregular spasms (contraction when it cannot be happening)
Attribute to organic pathology-psychological factors co-exist
Abrupt, stacccato, vocal explosions, strained-strangled, intermittent voice arrests on vowels
Larynx is normal at rest
Abductor
Severe breathy aphonia-intermittent arrests on voiceless consonants
VF episodically abduct to lateral position
Difficulty transition from voiceless consonant--> vowel
Mixed
Both AD and AB laryngospasms
Aphonic, breathy periods + voice arrests
What is it?
strained, choked effortful voice pattern
Relatively rare disorder
Resistant to traditional voice Tx
Medical mgm
Botox injections: thyroarytenoid, thyrovocalis for AD-SD ; to posterior cricoarytenoid for AB-SD
Results: muscle paralysis thru chemical denervation
Botox is neurotoxin-blocks transmission nerve impulses to muscle
Injected bilaterally via mouth or percutaneously in neck
Significant voice impv: 90% of normal fn (AD) ; 70% of normal fn (AB)
Airflow rates increase and normalise
Reduction intrinsic laryngeal muscle hyperfunction
Require re-injection every 3-4m
Other not well established medical options
Recurrent LN resection
Selective laryngeal AD denervation-reinnervation
Myotomy or myectomy
Type I/II thyroplasty
Autologus replacement of VF
Sodium oxybate: fast acting, effects are short lived, side effects are dose-dependent sedation and dizziness
Voice therapy is discredited and discarded for this population. Breathy voicing, elevation of pitch, reduces spasms, easy voice onsets, articulatory contacts, relaxation Tx, co-ordination exhalation, voice onset
Hypokinetic dysphonia
Aetiology: Parkinson's disease
Pathophysio
Varies depending on pt's age, duration, severity of the disease
VF normal in structure
Phonation: closure incomplete--> bowing of VF
X tense VF
Perceptual, physiological signs
Monopitch, monoloudness
Reduced loudness
Reduced stress
Harsh vocal quality
Breathiness
Increased airflow, decreased subglottal pressure
Mgm
Medical: Drug therapy, Parkinson's disease medication
Voice Tx
Increased VF adduction, increased loudness and intonation
LSVT
Expiratory muscle strength training: emerging area of research