Dysarthria 347
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Dysarthria
E Q Wang, Rush University Medical Center, Chicago, IL, USA
ã 2010 Elsevier Ltd. All rights reserved.
Glossary
Altered Auditory Feedback (AAF) – A collective
term for delayed auditory feedback (DAF),
frequency-altered feedback (FAF), and masking
noise, or a combination of the three.
Dysarthria – A group of speech disorders that are
due to lesions in either the peripheral or central
nervous system.
Festinating speech – A type of speech
characterized by increasingly fast and accelerated
speaking rate with diminished volume and
significantly reduced speech intelligibility. It is
commonly observed in patients with advanced PD
and Parkinsonism such as PSP or MSA. Patients
with festinating speech often experience festinating
gait and freezing of gait.
Lee Silverman Voice Treatment (LSVT/LOUD) –
An evidence-based treatment method for
hypophonia and hypokinetic dysarthria experienced
by 89% of patients with IPD. Its single treatment
target is loudness with high intensity in its delivery
mode and sensory retraining.
Speech intelligibility – The amount of speech that
can be understood by listeners who speak the same
language.
Definition and History
Speech problems experienced by persons with Parkinson’s
disease (PD) were first described in a case in 1817 by James
Remington G and Shitij K (2005) The Pharmacology of Atypical
Antipsychotics. In: Factor SA, Lang AE, and Weiner WJ (eds.) Drug
Induced Movement Disorders, 2nd edn., p. 55. Oxford: Blackwell
Publishing.
Schonecker M (1957) Ein eigentumliches syndrom im oralen bereich bei
megaphen applikation. Nervenartz 28: 35.
Tarsy D (1983) History and definition of tardive dyskinesia. Clinical
Neuropharmacology 6: 9199.
Tarsy D (2005) In: Factor SA, Lang AE, and Weiner WJ (eds.)
Miscellaneous Drug-Induced Movement Disorders, 2nd edn., p. 430.
Oxford: Blackwell Publishing.
Weiner WJ, Goetz CG, Nausieda PA, et al. (1978) Respiratory
dyskinesias: Extrapyramidal dysfunction and dyspnea. Annals of
Internal Medicine 88(3): 327–331.
Parkinson in his famous book ‘An Essay on the Shaking Palsy’.
The patient, the Count de Lordat, who suffered from a fall
three and half years earlier prior to the visit, was still able
to walk alone with a cane with great difficulty but had
limited range of motion of his upper limbs. He could not
control his saliva, drooling continuously. He had great
trouble swallowing liquids and could no longer swallow
solids. Although his mind was sound and he was able to
attend and understand conversations, ‘What words he still
could utter were monosyllables, and these came out, after
much struggle, in a violent expiration, and with such a low
voice and indistinct articulation, as hardly to be understood
but by those who were constantly with him.’ Speech impair-
ments such as this were termed as dysarthria. It comes from
the Greek prefix dys and the Greek root arthroun, while
‘dys’ means ‘bad or abnormal’ and ‘arthroun’ means ‘to
speak clearly.’
In their influential studies of the dysarthrias pub-
lished in 1969, Darley, Aronson and Brown used correla-
tion matrices to demonstrate for the first time that
cooccurrence of deviant speech dimensions observed
could be delineated into different types of dysarthria.
They further defined that ‘Dysarthria is a collective
name for a group of speech disorders resulting from dis-
turbances in muscular control over the speech mechanism
due to damage of the central or peripheral nervous sys-
tem. It designates problems in oral communication due
to paralysis, weakness, or incoordination of the speech
musculature. It differentiates such problems from disor-
ders of higher centers related to the faulty programm-
ing of movements and sequences of movements (apraxia
of speech) and to the inefficient processing of linguistic
units (aphasia).’
348 Dysarthria
Epidemiology/Risk Factors
Epidemiology as Related to Different Etiologies
Different underlying neurological disturbances are asso-
ciated with different types of dysarthria. However, speech
intelligibility is inevitably reduced in all. The dysarthria
classification was proposed in 1969 on the basis of lesion
sites. There are six single types of dysarthria: flaccid
dysarthria, spastic dysarthria, ataxic dysarthria, hypoki-
netic dysarthria, hyperkinetic dysarthria, and unilateral
upper motor neuron dysarthria, in addition to the cate-
gory of mixed dysarthria, which encompasses all possible
combinations of the six single types.
Dysarthria accounts for 54% of all acquired neuro-
logic communicative disorders. The prevalence of dys-
arthria in movement disorders is high. Hypokinetic
dysarthria is the dysarthria of idiopathic PD and atypical
Parkinsonism, while hyperkinetic dysarthria is associated
with involuntary movements as in Huntington’s disease
(HD). Eighty-nine percent of patients with idiopathic Par-
kinson‘s disease (IPD) have hypokinetic dysarthria. Mixed
hypokinetic–hyperkinetic dysarthria is commonly asso-
ciated with IPD, once patients develop on–off medication-
related motor fluctuations and dyskinesias. In patients with
atypical Parkinsonism such as progressive supranuclear
palsy (PSP) and multiple system atrophy (MSA), speech
impairment may be the first motor sign to appear. In PSP,
dysarthria occurs in 48–88% of patients, while in MSA, in
34–100%, depending on the disease progression. Hypoki-
netic dysarthria is seldom the only type of dysarthria
observed in atypical Parkinsonism. Mixed hypokinetic-
spastic dysarthrias are most commonly associated with
PSP, while mixed hypokinetic-ataxic-spastic dysarthrias
mostly seen in MSA. Hyperkinetic dysarthria occurs
when purposeful speech movement is interrupted by invol-
untary movements. Although it is identified as a single type
of dysarthria, there are shared features yet remarkable
differences in its actual speech characteristics, depending
on where and how the involuntary movements interfere
with speech movements. Any involuntary movements that
involve muscle groups in the trunk, head, and neck area will
likely cause hyperkinetic dysarthria. Hyperkinetic dysar-
thria is commonly associated with chorea in HD, palato-
pharyngolaryngeal myoclonus, tics in Tourette’s syndrome
(TS), dystonia involving head and neck muscles (cervical
dystonia, laryngeal dystonia, and oromandibular dystonia),
Essential tremor (ET), hemifacial spasm, tardive dyskine-
sias, and medication-induced dyskinesias.
Risk Factors
In idiopathic PD, the most important risk factors for
developing dysarthria are progression of the disease, dis-
ease severity level, and ‘on–off ’ motor fluctuations. In
atypical Parkinsonism, the most important risk factors
are presence of dysphagia, gait disturbances, and premor-
bid speech impairment. In movement disorders associated
with hyperkinetic dysarthria, the risk factors involve mus-
cle groups in the trunk, head, and neck area, and the
extent, frequency, and intensity of the involuntary move-
ments, as well as disease duration and progression.
Clinical Features/Diagnostic Criteria
Characterization
The main characteristic of any type of dysarthria is
the reduction of speech intelligibility. The severity of
hypokinetic dysarthria in PD is task dependent. The speech
intelligibility is worse with spontaneous speech than with
automatic speech such as counting, recitation, and reading
when the content of speech is provided. In more advanced
PD, the mixed hypokinetic–hyperkinetic dysarthria is
medication related. The hypokinetic component is worse
during ‘off ’ time, while the hyperkinetic component is
worse during ‘on’ time because of increased dyskinesias.
Salient Speech Features
Speech characteristics vary among different types of dys-
arthria. Salient speech features of hypokinetic dysarthria
in IPD progress from early symptoms such as reduced
loudness, monotone, monopitch, reduced pitch, and breathy
and hoarse voice quality, to relatively later symptoms such
as variable rate, short rushes of speech, hesitations, dis-
fluency similar to stuttering, palilalia which is speech pro-
duced with significantly accelerated speaking rate with
diminished volume, and significantly decreased articula-
tory accuracies. Hyperkinetic dysarthria associated with
involuntary movements is characterized by unpredictable
articulatory breakdowns and loudness and pitch variabil-
ity. Dysarthria associated with cervical dystonia often
manifests itself as spasmodic dysphonia. The salient speech
features are strained and strangled vocal quality and fre-
quent vocal arrests. Some patients may resolve to use
whispering voice. Other types of dysarthria commonly
associated with movement disorders are spastic dysarthria
and ataxic dysarthria. Spastic dysarthria presents with
strained–strangled vocal quality, low pitch, hypernasality,
slow but regular speaking rate, and effortful speech.
Ataxic dysarthria presents timing-related irregular artic-
ulatory breakdowns and variable pitch, loudness, and
speaking rate.
Diagnosis of Dysarthria
Certified and licensed speech-language pathologists
(SLP) are trained to diagnose dysarthria, using a combi-
nation of perceptual and instrumental tests to evaluate
respiration, phonation, articulation, resonance, and pros-
ody. A typical evaluation has the following components:

an in-depth medical history, a complete oral motor exam-
ination, and speech testing. On the basis of the findings,
the SLP will be able to differentially diagnose the type or
types of dysarthrias.
Pathophysiology
The precise pathophysiology underlying dysarthria in
IPD, atypical Parkinsonism and other movement disor-
ders is unclear. Rigidity and bradykinesia may be partially
responsible for hypokinetic dysarthria, while for hyperki-
netic dysarthria, the involuntary movements. Strained and
strangled vocal quality and slow but regular articulatory
movement patterns are consistent with increased spastic-
ity in the muscles in spastic dysarthria. Irregular articula-
tory breakdowns and irregular loudness and pitch of
ataxic dysarthria are consistent with dysfunction of the
cerebellum.
Management
Medication
Hypokinetic dysarthria of IPD may appear early or late
in the disease progression. The response to dopaminergic
stimulation in speech is mixed. Drug-induced orofacial
and respiratory dyskinesias interfere with speech move-
ments resulting in mixed hypokinetic–hyperkinetic dys-
arthria in IPD.
Deep Brain Stimulation
Bilateral deep brain stimulation (DBS) of the subthalamic
nucleus (STN) has gained increased acceptance, because
it substantially reduces dyskinesias and fluctuations and
improves the cardinal features of IPD. STN DBS does not
improve speech; rather, one of its common adverse effects
is worsened speech intelligibility. Speech deterioration
may be from two sources: the progression of the disease
itself and long-term stimulation-related changes. It has
been suggested that the contact site and stimulation inten-
sity may be partly responsible for the worsening speech.
Speech Therapy
Speech therapy that has demonstrated clear efficacy is
Lee Silverman Voice Treatment (LSVT/LOUD), an
intensive treatment program for treating hypophonia
and hypokinetic dysarthria in patients with IPD, targeting
a single treatment target of loudness with high intensity in
its delivery mode and sensory retraining. It works best
when the main symptoms are soft and breathy voice. More
advanced symptoms such as inability to initiate speech,
frequent hesitations, and palilalia have been reportedly
controlled by altered auditory feedback (AAF) provided
by a wearable device.
Dysarthria 349
Prognosis
Dysarthria in patients with IPD or other movement dis-
orders will worsen as the underlying disease progresses.
Early onset of severe speech deficits such as palilalia in
PD may indicate atypical Parkinsonism such as PSP or
MSA especially when dysphagia and gait disturbances
are present.
Acknowledgments
Emily Wang was supported by a research grant from the
Michael J. Fox Foundation for Parkinson’s Research.
See also: Alzheimer’s Disease and Parkinsonism; Ataxia;
Basal Ganglia, Functional Organization; Cognitive Assess-
ments and Parkinson’s Disease; Corticobasal Degenera-
tion; Deep Brain stimulation; Dyskinesias; Dystonia; Hoehn
and Yahr Staging Scale; Huntington’s Disease; Levodopa;
Multiple System Atrophy; Pallidotomy for Parkinson’s
Disease; Parkinson’s Disease: Definition, Diagnosis, and
Management; Progressive Supranuclear Palsy; Spasmodic
Dysphonia: Focal Laryngeal Dystonia; Surgery for Move-
ment Disorders, Overview, Including History; Unified
Parkinson’s Disease Rating Scale (UPDRS) and The
Movement-Disorder Society Sponsored-unified Parkin-
son’s Disease Rating Scale (MDS-UPDRS); Wilson’s
Disease.
Further Reading
D’Alatri L, Paludetti G, Contarino MF, Galla S, Marchese MR, and
Bentivoglio AR (2008) Effects of bilateral subthalamic nucleus
stimulation and medication on Parkinsonian speech impairment.
Journal of Voice 22: 365–372.
Darley F, Arnold A, and Brown J (1975) Motor Speech Disorders. Lehigh
Acres: WB Saunders.
Darley F, Aronson A, and Brown J (1969a) Clusters of deviant speech
dimensions in the dysarthrias. Journal of Speech and Hearing
Research 12: 462–496.
Darley F, Aronson A, and Brown J (1969b) Differential diagnostic patterns
of dysarthria. Journal of Speech and Hearing Research 12: 246–269.
Duffy J (2005) Motor Speech Disorders: Substrates, Differential
Diagnosis, and Management. St. Louis: Mosby.
Goetz CG, Leurgans S, Lang AE, and Litvan I (2003) Progression of gait,
speech and swallowing deficits in progressive supranuclear palsy.
Neurology 60: 917–922.
Kent R, Kent J, Duffy J, and Weismer G (1998) The dysarthrias: Speech-
voice profiles, related dysfunctions, and neuropatholgy. Journal of
Medical Speech-Language Pathology 6: 165–211.
Klostermann F, Ehlen F, Vesper J, et al. (2008) Effects of subthalamic
deep brain stimulation on dysarthrophonia in Parkinson’s disease.
Journal of Neurology, Neurosurgery, and Psychiatry 79: 522–529.
Logemann J, Fisher H, Bashes B, and Blonsky E (1978) Frequency and
co-occurrence of vocal rate dysfunction in the speech of a large
sample of Parkinson patients. Journal of Speech and Hearing
Disorders 43: 47–57.
McNeil MR (2008) Clinical Management of Sensorimotor Speech
Disorders, 2nd edn. New York: Thieme.
350 Dyskinesias
Nebel A, Reese R, Deuschl G, Mehdorn HM, and Volkmann J (2009)
Acquired stuttering after pallidal deep brain stimulation for dystonia.
Journal of Neural Transmission 116: 167–169.
Pinto S, Gentil M, Krack P, et al. (2005) Changes induced by levodopa
and subthalamic nucleus stimulation on Parkinsonian speech.
Movement Disorders 20: 1507–1515.
Pinto S, Ozsancak C, Tripoliti E, Thobois S, Limousin-Dowsey P, and
Auzou P (2004) Treatments for dysarthria in Parkinson’s disease.
Lancet Neurology 3: 547–556.
Ramig LO, Fox C, and Sapir S (2008) Speech treatment for Parkinson’s
disease. Expert Review of Neurotherapeutics 8: 297–309.
Videnovic A and Verhagen Metman L (2008) Deep brain stimulation for
parkinson’s disease: Prevalence of adverse events and need for
standardized reporting. Movement Disorders 23: 343–349.
Wang E, Verhagen Metman L, Bakay R, Arzbaecher J, and Bernard B
(2003) The effect of unilateral electrostimulation of the subthalamic
nucleus on respiratory/phonatory subsystems of speech production
in Parkinson’s disease – A preliminary report. Clinical Linguistics and
Phonetics 17: 283–289.
Wang EQ, Verhagen Metman L, Bakay RAE, Arzbaecher J,
Bernard B, and Corcos DM (2006) Hemisphere-specific effects of
Dyskinesias
O Rascol, University Paul Sabatier, Toulouse, France; University Hospital, Toulouse, France
N Fabre, University Hospital, Toulouse, France
C Brefel-Courbon, University Paul Sabatier, Toulouse, France; University Hospital, Toulouse, France
F Ory-Magne, University Hospital, Toulouse, France
S Perez-Lloret, University Paul Sabatier, Toulouse, France; University Hospital, Toulouse, France
ã 2010 Elsevier Ltd. All rights reserved.
Glossary
Basal ganglia – The basal ganglia are neurons
nuclei located at the brain base, comprising the
substantia nigra, the striatum, the internal and
external segments of the globus pallidus, and the
subthalamic nucleus (STN) ganglia and playing a key
role in the control of motor behavior through their
in- and outputs.
Continuous dopaminergic stimulation – The
mode of administration (pulsatile versus continuous)
of dopaminergic antiparkinsonian medications
seems crucial in the development of LIDs. Normal
endogenous striatal dopamine receptor stimulation is
supposed to be phasic and tonic at the level of a
synapse, with a relatively stable continuous baseline
release. Short acting drugs (such as levodopa)
induce an abnormal pulsatile stimulation that disturbs
the striatal relay of the motor system. Exposing an
increasingly denervated striatum to pulsatile
dopaminergic stimulation might then induce
dyskinesia.
Deep brain stimulation – Chronic high frequency
stimulation mimics the effects of ablative
neurosurgery. This stimulation is obtained by means
of an electrode with four contacts implanted into the
subthalamic nucleus deep brain stimulation on speaking rate
and articulatory accuracy of syllable repetitions in Parkinson’s
disease. Journal of Medical Speech-Language Pathology
14: 323–333.
Wang EQ, Verhagen Metman L, and Bernard B (2008) Treating
festinating speech with altered auditory feedback in Parkinson’s
disease: A preliminary report. Journal of Medical Speech-Language
Pathology 16: 275–282.
Relevant Websites
http://www.asha.org – American Speech-Language-Hearing
Association (ASHA).
http://www.michaeljfox.org – The Michael J. Fox Foundation for
Parkinson’s Research.
http://www.nidcd.nih.gov – National Institute on Deafness and Other
Communication Disorders (NIDCD).
http://www.lsvt.org – LSVT GlobalW.
target area and connected to a programmable
stimulator under the chest wall.
Diphasic dyskinesias or ‘onset- and end-of-
dose-dyskinesias’ – Diphasic dyskinesias correlate
respectively with the rising and falling phases of
levodopa plasma levels, can involve stereotypical
rapid alternating movements, as well as unusual
ballistic kicking or dystonia and tend to affect the legs
predominantly.
Dyskinesias – Dyskinesias are abnormal
involuntary hyperkinetic movements commonly
observed in patients with PD chronically treated with
levodopa (levodopa induced dyskinesias (LIDs)) and
rarely with dopaminergic agonists.
Off dystonia – Off dystonia is painful dystonic
posturing affecting the limbs particularly the legs and
feet, occurring at the end of action of levodopa in
levodopa-treated parkinsonian patients.
Peak-dose dyskinesias – Peak dose dyskinesias
are the most common LIDs. They occur at the time of
the peak concentration or peak benefit of the dose of
levodopa when parkinsonian symptoms are
improved. Typically, peak-dose dyskinesias involve
the upper limbs more than the legs, trunk, or head
and have a choreic phenotype.