neurogenic voice disorders courtney lippe kristina curro

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Neurogenic Voice Disorders Courtney Lippe Kristina Curro

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Neurogenic Voice Disorders

Courtney LippeKristina Curro

Organic Voice Disorders

• Structural: involve something physically wrong with a speech mechanism.

• Neurogenic: are caused by a problem with the CNS or PNS.

Spasmodic Dysphonia

• “SD is characterized by abnormal involuntary movements that are action induced and task specific” Stemple et al.

• Movement during vocalization that produces involuntary co-contraction of the muscles used to produce sound.

• Normal structure!

Spasmodic Dysphonia• 3 types : Adductor vs. Abductor and rare form of

mixed dysphonia

• Recent evidence suggest that it is a focal dystonia of the CNS

• Extrapyramidal in origin

• Supranuclear lesion locus in area of the Basal Ganglia

Spasmodic Dysphonia:Complaints

• Poor vocal quality• Loss of vocal control• Rapid fatigue and strain involved in speech• Cannot be understood due to decrease in

intelligibility

Spasmodic Dysphonia

• Diane Rehm NPR talk radio voice

Spasmodic Dysphonia Treatments:

• Midline type 2 Thyroplasty (surgical)

• Sectioning or removal of the recurrent laryngeal nerve (surgical)

• Botox injection

• Chiropractics (derotation of 1st and 2nd vertebrae)

• Behavioral therapy

Midline type 2 Thyroplasty

Benign Essential Tremor

• Neurologic movement disorder that primarily involve upper body and limbs but can also involve head, voice, tongue or palate

• Not related to any other disease process

• Usually absent at rest

• Average age of onset 45 years

Benign Essential Tremor

Katherine Hepburn

Benign Essential Tremor : Complaints

• Poor vocal quality

• “old sounding voice”

• Decrease in volume

• Fatigue with vocal use

Benign Essential Tremor :

• Team: neurologist, otolaryngologist and speech Language Pathologist

• There is no cure for organic voice tremor but the symptoms can be treated.

• Botox is an option if there is co-occuring spasticity

• Speech therapy to improve respiratory support• Prognosis: poor

Current Therapy :

• Beta-adrenergic blockers(medication)• Primidone(medication)• Benzodiazepines(medication)• Botulinum A(injections)• Alcohol• Thalamotomy(surgical)• Thalamic Stimulation(surgical)• Non-Pharmacologic Treatment

Neurogenic Vocal Fold Paralysis

Figure 5. Unilateral vocal cord paralysis. (Left) Larynx in abduction. (Right) Larynx in adduction, showing paralyzed vocal cord (arrow).

Vocal Fold Paralysis:

• Nerve impulses to the vocal folds are either partially or completely interrupted which results in limited or no movement of the muscles of the larynx.

• Can occur at any age

• Results: Voice changes, problems with airway, dysphagia

Complaints:

• Hoarseness• Breathy• Diplophonia• Shortness of breath• Stridor• Ineffective cough• Coughing or choking with food• globus sensation

Neurologic Causes:

• Arnold-Chiari malformation• Meningomyelocele• Diabetes mellitus• Amyotrophic lateral sclerosis• Myasthenia Gravis• Mobius syndrome• Charcot-Marie-Tooth syndrome• Postpolio syndrome• Lyme Disease

Medical Therapy:

• Corticosteroids work for some conditions

• Glucose management for diabetes

• Reflux medication

Parkinsons’s Disease/Parkinsonism/resulting in Hypokinetic Dysarthria

• Cause/Site of lesion: Degeneration of the substantia nigra, causing a decrease in the amount of dopamine in the brain and thereby inhibiting movement.

• Drug-induced, such as exposure to heroin• Post-encephalitic, thought to be due to exposure

to a virus, although evidence is weak at best.• Idiopathic, possibly due to the aging process or

heredity.

Vocal quality complaints:

• Hard to get speech started

• Quiet or weak voice

• Fatigue during speech

• Reports “stuttering”, or repeating sounds or words.

• Hypokinetic dysarthria voice characteristics (Duffy, 2005):

Phonation

• Mono-pitch• Mono-loudness• Harsh Voice Quality• Breathy voice• Low pitch (reduced f0)• Reduced intensity• Voice tremor• Increased jitter/shimmer

Respiration:

• Reduced maximum vowel prolongation• Reduced airflow• Reduced respiratory excursions• Reduced vital capacity• Paradoxical respiratory movements

Articulation/Prosody:

• Reduces Stress• Imprecise Consonants• Variable Rate• Repeated phonemes• Inappropriate pauses• Continued voicing during voiceless consonants

Resonance:

• Increased nasalization is possible, but usually normal.

Laryngeal Characteristics:

• Bowed vocal folds despite solid, non-flaccid appearance

• Tremulousness of arytenoid cartilages

• Asymmetry of structure movement

Treatment options and effectiveness

• LSVT to promote volume and breath support (Ramig and Verdolini, 1996)

• Prosodic exercises (as reported in Scott and Caird, 1983, from Ramig and Verdolini, 1996)

Drug Treatment

• Most drug treatment is for PD in general, not specifically for treatment of the voice disorder itself.

• levodopa-carbidopa (dopamine precursors), bromocriptine (dopamine agonist) etc. (Kolb and Wishaw, 1996)

Surgical Treatment:• Collagen injection into vocal folds (Sewall et al.

2006) to improve glottal closure. Pt. subjectively reported improvement of vocal quality (Vocal Handicap Index), and objective CAPE-V measurements also showed improvement. However, small sample size and short duration of monitoring.

• Deep brain stimulation and fetal cell transplantation were shown to help reduce overall symptoms of PD, but had a negative impact on speech quality (Trail et al. 2005)

Other Treatments:

• Transcranial Magnetic Stimulation (Dias et al., 2006) showed that stimulating the primary motor cortex (M1)-mouth area provided objective and subjective improvements in speech and may be used in future treatment.

Prognosis:

• New research suggests a combination of LSVT and collagen injections may provide the greatest improvement to voice quality.

Flaccid Dysarthria

• Cause/Site of lesion: Lower motor neuron involvement. In Myasthenia Gravis (MG): Failure of neuromuscular transmission wherein acetylcholine degrades too quickly because the immune system attacks its own AchRs. This lack of Ach reaching the neuronal terminals causes flaccid dysarthria that recovers after a period of rest.

Complaints:

• Breathy or quiet voice, inability to move articulators

• In MG: Weakness and fatigue after muscle use, for example, weakness increases towards the end of a conversation, and recovers with a period of rest

Phonation:

• Breathiness

• Short phrases

• Audible inspiration

Respiration:

• Insufficient breath support, although isolated respiration difficulty is rare.

• Poor posture

• Reduced exhalation control• Slow breathing

Articulation/Prosody

• Harsh voice

• Monoloudness

• Monopitch

Resonance:

• Imprecise consonants (although this occurs with may other dysarthrias)

• Increased nasalization and nasal emission (may be the first sign of ALS)

Treatment options and effectiveness:

• MG: General treatment includes thymectomy to reduce antibody formation, but it’s effect on voice treatment specifically is not addressed.

• Thyroplasty: surgery to enhance function of the larynx

• Palatal lifts if the velum is affected

Ataxic dysarthria

• Location/site of lesion: bilateral cerebellar involvement

• Complaints of patient: imprecise articulation, laborious speech, may be observed groping for sounds, sound substitution

Phonation:

• Breathy• Hoarse• Tremor• Mono-pitch• Mono-loudness

Respiration:

• Shallow inhalation and reduced exhalation control

• Rapid breaths

• Irregular and suddenly forced patterns

Articultion/Prosody

• Imprecise, slow and irregular

• Explosive syllable stress

• Explosive loudness, outbursts

• Abnormal prolongations of phonemes

Treatment options and effectiveness:

• Intense phonomotor treatment (Kendall et al. 2006): in a single case study found that intense phonomotor treatment increased ease of production of single sounds but generalization to connected speech did not occur.

References• Cannito, Michael P. et al. Perceptual Analysis of Spasmodic Dysphonia Before

and After. Arch Otolaryngol Head Neck Surg.,130:1393-1399• Daya, Hamid FRCS et al.(2006) Pediatric Vocal Fold Paralysis. Arch Otolaryngol

Head Neck Surg.,vol 126:21-25• Dias, A.E., Barbosa, E.R., Coracini, K., Maia, F., Marcolin, M. A., Fregni, F.

(2006). “Effects of repetitive transcranial magnetic stimulation on voice and speech in Parkinson's disease.” Acta Neurologica Scandinavica. 113(2), 92-99

• Duffy, J.R. (2005). Motor Speech Disorders: Substrates, Differential Diagnosis, and Management. Elsevier Mosby : St. Louis.

• Dworkin, J.P. (1991). Motor Speech Disorders. Mosby: New York.• Dysphonia by Surgical Myectomy : A Preliminary Report. Annals of Otology,

Rhinology & Laryngology. 115(2):97-102, 2006.

References• Kendall, D.L., Rodriguez A.D., Rosenbek, J.C., Conway T., Gonzalez

Rothi L.J.“Influence of intensive phonomotor rehabilitation on apraxia of speech.” Journal of Rehabilitation Research and Development. 43(3). 409-18

• Kolb, B., Wishaw, I.Q. (1996). Fundamentals of Human Neuropsychology – 4th Edition. W.H. Freeman Company : New York.

• Neurogenic dysphonia (1994). Ann Otol Rhinol Laryngol. Jan-Feb;93(1 Pt 1):57-64. PMID: 6703599 [PubMed - indexed for MEDLINE]

• Rajish, Pahwa. (2003) “Essential Tremor: differential diagnosis and current therapy”. The American Journal of Medicine. 115(2), 134-142

References• Ramig, L.O., Verdolini, K. (1998). “Treatment Efficacy, Voice

Disorders”. Journal of Speech, Language, and Hearing Research. 41(1), S101 – S116.

• Sapienza CM, Murry T, Brown WS (1998) Variations in adductor spasmodic dysphonia: Acoustic evidence. J Voice, 12(2): 214-222

• Stemple, J.C., Glaze, L.E., Klaben, B.G. (2000). Clinical Voice Pathology- Third Edition. Singular Publishing Group: Canada.

• Sewall G.K., Jiang J., Ford C.N. (2006). “Clinical evaluation of Parkinson’s –related dysphonia”. Laryngoscope. Oct;116(10):1740-4

• Trail, M., Fox, C., Ramig, L.O., Sapire, S., Howard, J, and Lai, E.C. (2005). “Speech treatment for Parkinson’s Disease”. NeuroRehabilitation. 20, 205–221.

• http://www.parkinsonsdisease-rhodeisland.org/Treating%20the%20voice.htm as retrieved on 3/1/2007.